Defense Cancer

What is Lymphoma Cancer?

2010-08-15T10:24:00.000-07:00

The lymphatic system is comprised of the lymph, lymph vessels, lymph nodes, bone marrow, spleen, and liver. The lymph is the fluid that circulates in the lymphatic system and travels through the body via lymph vessels. The fluid contains lymphocytes - produced by the bone marrow and spleen -that fight pathogens. These cells filter the blood and collect the microorganisms inside lymph nodes. You'll notice that during infections, you will have a palpable node in your neck, under your arms, breasts, and groin. When the pathogens are overwhelmed, toxins and byproducts produced by these cells are then filtered in the liver to be eliminated.

In lymphoma cancer, the problem lies in the lymphocytes, specifically the B-lymphocytes and T-lymphocytes. Hodgkin's lymphoma is a type of lymphoma cancer where the B-lymphocytes have the presence of Reed-Sternberg cells under morphological studies. Non-Hodgkin's lymphoma, on the other hand, is a type of lymphoma that occurs without the presence of Reed-Sternberg cells. The malignant cells increase in number and size, resulting to a pooling of cells inside a lymph node. The lymph node formed will be rubbery, painless, and does not show any signs of disappearing. Lymphoma cancer is also noted with night sweats, unexplained weight loss, and unexplained fever. There are patients diagnosed with lymphoma but still live for more than 5 to 10 years, making this one of the most curable forms of cancer known to man. Biopsy of the tumor is the definitive way in diagnosing lymphoma. Imaging tests such as X-Ray, CT-Scan, and MRI along with blood tests are done in order to stage the severity of lymphoma cancer.

Treatment of lymphoma cancer can be a form or mix of radiation therapy and chemotherapy. Radiation therapy is done during the early stage, and applied only on a local area where the malignancy is noted. When the malignancy has spread in adjacent and distal parts of the body, chemotherapy is used along with immune-stimulants and corticosteroids such as prednisone. Surviving lymphoma is highly dependent on the stage when the lymphoma was diagnosed and the application of appropriate treatment. Always maintain your regular check up to see if your treatment is appropriate for you, and to monitor how the lymphoma cancer is progressing.

Three Main Types of Mesothelioma

2010-08-08T05:51:00.000-07:00

Exposure to asbestos can lead to a number of long-lasting and even fatal disorders such as pleural plaques, asbestos warts, and lung cancer. Additionally, a specific type of cancer, called mesothelioma is almost always caused by asbestos. This deadly cancer comes in three different forms that attacks the membranes of the body.

Asbestos can be a wonderfully helpful mineral as long as it does not flake off into microscopic airborne fibers, which can then become lodged in your body. The reason why this mineral became so popular is because it is a silicate mineral. Silicates are highly resistant to a number of different things, including heat, chemicals, flame, electricity, and degradation. Additionally, asbestos itself is characterized by high tensile strength and flexibility.

Because of this, asbestos was a prominent component of many different materials for most of the 20th century. It could be found in ceiling tiles, brake pads, stage curtains, vinyl flooring, and more. However, doctors in a South African town near asbestos mines recognized a lung disease that was not responding to tuberculosis medication. After several years of research, they determined that they had found a new type of cancer caused by asbestos exposure, called mesothelioma. They published their findings in the late 1950s, and now we have discovered even more about this disease.

Mesothelioma is a particular form of cancer that attacks the inner linings of the body. Serous membranes line things like organs and are important because they secrete a special fluid that keeps friction from wearing away at your insides. There are three prominent serous membranes in the body, with other smaller ones scattered throughout. Thus, mesothelioma can originate in any of these.

First, pleural mesothelioma is the primary form of the disease. It attacks the lining of the lungs, causing an accumulation of fluid between the lungs and the lung cavity. This leads to symptoms like coughing, difficulty breathing, shortness of breath, and weight loss.

Next, the type of mesothelioma that harms the stomach and abdomen is called peritoneal mesothelioma. Doctors believe that ingested asbestos fibers contribute to this disease, which causes tumors to build up along the walls of the abdomen. This can cause things like pain, nausea, vomiting, and bowel obstruction. Additionally, peritoneal mesothelioma can spread into the testicles, which are surrounded by an extension of the peritoneal membrane.

Lastly, pericardial mesothelioma affects the lining that surrounds the heart. This is the rarest form of this cancer, and it also causes tumors that lead to a buildup of fluid around the heart. This can disrupt the heart's function, which can lead to chest pain and palpitations.

Whatever form of this cancer someone has, it can be extremely painful and also fatal. If you or someone you love is suffering from this terrible disease, you should talk to a lawyer about your options. For more information, check out the mesothelioma attorneys at the firm of Williams Kherkher today.

The 4 Main Types of Mesothelioma - A Closer Look at How They Are Different

2010-08-08T05:49:00.000-07:00

Mesothelioma is the general term used for any type of cancer that occurs in the mesothelium, which is the tissue that surrounds one's vital organs. While all forms of mesothelioma are a result of exposure to asbestos, a toxic chemical found in many locations, there is more than one type of this form of cancer.

As the mesothelium tissue can be found in many parts of the body, the cancer that develops in this tissue can also be found in different areas. Accordingly, there are four types of mesothelioma currently recognized by medical professionals: testicular, pericardial, peritoneal, and pleural. These names refer to the area of the body in which the cancer is concentrated.

Testicular Mesothelioma

Testicular refers to the testicles, so this form of mesothelioma affects the tissue found in this part of the male anatomy. This is the least common form of the disease, and as such, there is not a great deal of information available on prevalence statistics or common treatments. There have been less than one hundred cases of this type of mesothelioma reported at this point.

Pericardial Mesothelioma

Also one of the more rare forms of mesothelioma, pericardial mesothelioma affects the mesothelium found around the heart. The symptoms, which include a persistent cough, heart palpitations, shortness of breath, problems breathing, and chest pain, are difficult to differentiate from those of pleural mesothelioma.

Peritoneal Mesothelioma

The peritoneum refers to the lining of the abdominal cavity, which is why the cancer that occurs in this tissue is referred to as peritoneal mesothelioma. This cancer affects the tissues surrounding the organs found in the abdomen, including the stomach and intestines. Peritoneal mesothelioma is more common than either testicular or pericardial mesothelioma, accounting for somewhere between ten and twenty percent of the total number of mesothelioma cases reported. Some symptoms of this form of cancer include pain or swelling in the abdomen, bowel issues, anemia, problems breathing, nausea, blood clotting, loss of appetite, vomiting, and chest pains.

Pleural Mesothelioma

Approximately three quarters of all mesothelioma cases are pleural mesothelioma, making this the most common type of the disease. This type of cancer is concentrated in the tissues around the lungs and those that line the cavity in which the lungs are located. Patients with pleural mesothelioma notice symptoms because fluid builds up between the wall of the chest cavity and the lungs, which makes it harder for the lungs to function properly. Common symptoms of pleural mesothelioma include finding it hard to breath, pains in the chest area, and a persistent cough.

Can Black People Get Skin Cancer?

2010-07-23T19:21:00.000-07:00

Skin cancer is the most common of all the cancers. For years, the majority of the black population and even many medical specialists have assumed that people of color cannot get skin cancer, but that assumption is very much false.

Believing themselves safe from the sun's radiation, many people with darker complexions do not use sunscreen. Since these individuals feel invincible against the sun, they often are unaware of the symptoms of cancer of the skin when they are present. As a result, even though this cancer can be treated, is more likely to result in fatalities in cases involving people with darker skin tones than people with lighter skin tones. This is because usually when skin cancer is diagnosed in persons with brown or black skin, the cancer is typically in its later stages. At this point, the cancer may have spread and be impossible to treat.

Signs of skin cancer in darker individuals are typically seen in body areas which have less skin color such as fingers, soles, the palms of the hands, and toes. Symptoms sometimes even appear in the mouth and near the reproductive organs.

While a high percentage of Caucasians wear sunscreen when they're exposed to the sun for long periods of time, the percentage of people of color who wear sunscreen is estimated to be less than thirty percent. To alleviate the risks of skin cancer, all individuals, regardless of race, should wear sunscreen.

Cancer of the skin does not discriminate; it affects people of all races. Therefore, everyone should take preventive measures to avoid the sun's UV rays and see a physician at the first appearance of a mole or an abnormal growth. Just because skin cancer does occur less often in people of color, this does not mean that this group is invulnerable to cancer.

Broccoli

2010-06-28T03:55:00.000-07:00

Broccoli (from the Italian plural of broccolo, referring to "the flowering top of a cabbage")is a plant of the mustard/cabbage family Brassicaceae (formerly Cruciferae). It is classified in the Italica cultivar group of the species Brassica oleracea. Broccoli has large flower heads, usually green in color, arranged in a tree-like fashion on branches sprouting from a thick, edible stalk. The mass of flower heads is surrounded by leaves. Many varieties of broccoli are perennial. Broccoli most closely resembles cauliflower, which is a different cultivar group of the same species.

History
Broccoli evolved from a wild cabbage plant on the continent of Europe. Indications point to the vegetable's being known 2,000 years ago.Since the Roman Empire, broccoli has been considered a uniquely valuable food among Italians.[5] Broccoli was first introduced to the United States by these immigrants, but did not become widely known until the 1920s

Uses
Culinary
Broccoli is usually boiled or steamed, but may be eaten raw and has become popular as a raw vegetable in hors d'œuvre trays. Although boiling has been shown to reduce the levels of suspected anti-cancer compounds in broccoli, other preparation methods such as steaming, microwaving, lactic fermentation, and stir-frying have not been shown to reduce the presence of these compounds

Nutritional and medicinal
Broccoli is high in vitamins C, K, and A, as well as dietary fiber; it also contains multiple nutrients with potent anti-cancer properties, such as diindolylmethane and small amounts of selenium.A single serving provides more than 30 mg of Vitamin C and a half-cup provides 52 mg of Vitamin C.The 3,3'-Diindolylmethane found in broccoli is a potent modulator of the innate immune response system with anti-viral, anti-bacterial and anti-cancer activity.Broccoli also contains the compound glucoraphanin, which can be processed into an anti-cancer compound sulforaphane, though the benefits of broccoli are greatly reduced if the vegetable is boiled more than ten minutes.A high intake of broccoli has been found to reduce the risk of aggressive prostate cancer.Broccoli consumption has also been shown to be beneficial in the prevention of heart disease

Varieties
There are three commonly grown types of broccoli. The most familiar is called "calabrese" in Great Britain and simply "broccoli" in North America. It has large (10 to 20 cm) green heads and thick stalks and is named after Calabria in Italy. It is a cool season annual crop.

Sprouting broccoli has a larger number of heads with many thin stalks. It is planted in May to be harvested during the winter or early the following year in temperate climates. The heirloom variety "calabrese" available in North America is of this type.

Romanesco broccoli has a distinctive fractal appearance of its heads, and is yellow-green in colour. It is technically in the Botrytis (cauliflower) cultivar group.

Purple cauliflower is a type of broccoli sold in southern Italy, Spain, and the United Kingdom. It has a head shaped like cauliflower, but consisting of tiny flower buds. It sometimes, but not always, has a purple cast to the tips of the flower buds.

Other cultivar groups of Brassica oleracea include cabbage (Capitata Group), cauliflower (Botrytis Group), kale and collard greens (Acephala Group), kohlrabi (Gongylodes Group), and Brussels sprouts (Gemmifera Group). Chinese broccoli (Alboglabra Group) is also a cultivar group of Brassica oleracea

Production

Cauliflower and broccoli output in 2005In North America, production is primarily in California. The seasonal average f.o.b. shipping-point price for cauliflower in 2004 was $33.00 per 100 pounds ($0.73/kg) according to the National Agricultural Statistics Service, USDA

Cancer

2010-06-06T09:28:00.000-07:00

Broccoli With Garlic

2010-01-30T19:49:00.000-08:00

Ingredients:

* 16 ounces broccoli florettes
* 1 tablespoon butter
* 1 tablespoon roasted walnut oil or olive oil
* 2 cloves garlic, finely minced
* 1/4 cup finely chopped red onion
* 2 teaspoons lemon juice
* 1/2 teaspoon salt
* Dash black pepper

Preparation:

Steam the broccoli just until tender.

In a small saucepan, heat the butter and oil; add minced garlic, red onion, and lemon juice. Cook just until tender. Toss with the broccoli along with the salt and pepper. Taste and adjust seasonings.
Serves 4.

Breast Cancer Surgery: Lumpectomy, Mastectomy

2010-01-09T00:56:00.000-08:00

How to beat cancer Part 3

2009-12-18T19:24:00.002-08:00

How to beat cancer Part 1

2009-12-18T19:24:00.001-08:00

How to beat cancer Part 2

2009-12-18T19:23:00.000-08:00

we'll beat cancer liver cancer

2009-12-18T19:22:00.000-08:00

Causes of cancer

2009-09-21T00:21:00.000-07:00

Cancer is a diverse class of diseases which differ widely in their causes and biology. Any organism, even plants, can acquire cancer. Nearly all known cancers arise gradually, as errors build up in the cancer cell and its progeny (see mechanisms section for common types of errors).

Anything which replicates (our cells) will probabilistically suffer from errors (mutations). Unless error correction and prevention is properly carried out, the errors will survive, and might be passed along to daughter cells. Normally, the body safeguards against cancer via numerous methods, such as: apoptosis, helper molecules (some DNA polymerases), possibly senescence, etc. However these error-correction methods often fail in small ways, especially in environments that make errors more likely to arise and propagate. For example, such environments can include the presence of disruptive substances called carcinogens, or periodic injury (physical, heat, etc.), or environments that cells did not evolve to withstand, such as hypoxia[5] (see subsections). Cancer is thus a progressive disease, and these progressive errors slowly accumulate until a cell begins to act contrary to its function in the animal.

The errors which cause cancer are often self-amplifying, eventually compounding at an exponential rate. For example:

A mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate errors more rapidly
A mutation in signaling (endocrine) machinery of the cell can send error-causing signals to nearby cells
A mutation might cause cells to become neoplastic, causing them to migrate and disrupt more healthy cells
A mutation may cause the cell to become immortal (see telomeres), causing them to disrupt healthy cells forever
Thus cancer often explodes in something akin to a chain reaction caused by a few errors, which compound into more severe errors. Errors which produce more errors are effectively the root cause of cancer, and also the reason that cancer is so hard to treat: even if there were 10,000,000,000 cancerous cells and one killed all but 10 of those cells, those cells (and other error-prone precancerous cells) could still self-replicate or send error-causing signals to other cells, starting the process over again. This rebellion-like scenario is an undesirable survival of the fittest, where the driving forces of evolution itself work against the body's design and enforcement of order. In fact, once cancer has begun to develop, this same force continues to drive the progression of cancer towards more invasive stages, and is called clonal evolution.

Research about cancer causes often falls into the following categories:

Agents (e.g. viruses) and events (e.g. mutations) which cause or facilitate genetic changes in cells destined to become cancer.
The precise nature of the genetic damage, and the genes which are affected by it.
The consequences of those genetic changes on the biology of the cell, both in generating the defining properties of a cancer cell, and in facilitating additional genetic events which lead to further progression of the cancer

Signs and symptoms of cancer

2009-09-21T00:18:00.000-07:00

Roughly, cancer symptoms can be divided into three groups:

Local symptoms: unusual lumps or swelling (tumor), hemorrhage (bleeding), pain and/or ulceration. Compression of surrounding tissues may cause symptoms such as jaundice (yellowing the eyes and skin).
Symptoms of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis, hepatomegaly (enlarged liver), bone pain, fracture of affected bones and neurological symptoms. Although advanced cancer may cause pain, it is often not the first symptom.
Systemic symptoms: weight loss, poor appetite, fatigue and cachexia (wasting), excessive sweating (night sweats), anemia and specific paraneoplastic phenomena, i.e. specific conditions that are due to an active cancer, such as thrombosis or hormonal changes.
Every symptom in the above list can be caused by a variety of conditions (a list of which is referred to as the differential diagnosis). Cancer may be a common or uncommon cause of each item.

Chronic Diseases: Who's killing us, and how?

2009-08-31T17:41:00.000-07:00

Sodium bicarbonate, a natural way to treat the cancer

2009-08-13T01:34:00.000-07:00

Cancer Biology 101: Advances in Prostate Cancer

2009-08-07T18:06:00.000-07:00

Breast cancer

2009-07-04T20:20:00.000-07:00

· Breast cancer is the second most common form of cancer in women and one out of every nine women will develop breast cancer.
· Breast cancer is almost four times more likely to occur in a woman who has a mother or sister with breast cancer.
Most breast cancers are found by patients and not doctors.

· Risk factors for breast cancer
The biggest risk factor for breast cancer is a family member with a history of breast cancer.

Other risk factors include:

previous fibrocystic breast disease
previous uterine cancer
diets which are high in fat
estrogen replacement after menopause
postmenopausal women who use estrogen and progesterone have a significantly increase risk of
developing breast cancer compared with estrogen alone
alcohol may increase the risk of breast cancer

· Screening for breast cancer
Women should perform self breast examinations every month about a week after their menstrual cycle.
Women should have a yearly breast examination by their doctor.
Screening mammograms should be preformed every year starting at age 40.
MRI imaging and breast ultrasound are good screening tests for women with a high risk of breast cancer or in women who have an abnormal mammogram.

· Symptoms of Breast Cancer
A single or solitary breast mass is the most common sign of breast cancer. A breast cancer mass will typically be non-tender and firm or hard.

· Other sign of breast cancer may include:
· breast pain
· changes in the size of the breast such as breast swelling, breast edema
· breast shrinkage
· increase in firmness of the breast
· changes in the skin of the breast
· rash of the breast
· changes in the nipple such as a nipple rash, scaling or nipple discharge
· nipple itch or burning
· Swollen lymph node in the under arm area
· unexplained weight loss

· Types of Breast Cancer

There are two basic types of breast cancer:

Lobular cancinoma is breast cancer of the breast tissue.
Ductal carcinoma is breast cancer of the ducts in the breast. Breast cancer of breast ducts in more common.
Breast cancer may have receptors for progesterone or estrogen.

· Treatment
Treatment for breast cancer depends on the type of breast cancer, staging and presence of estrogen or progesterone receptors.

Treatment may include surgery, medication and radiation therapy.

· Prognosis
Breast cancer has a very good prognosis if it is localized to the breast and has not spread, and treatment can cure up to 90% of these cases of breast cancer.

Treating Cancer (Cancer #4)

2009-06-10T03:49:00.002-07:00

Risk Factors for Cancer (Cancer #2)

2009-06-10T03:49:00.001-07:00

Understanding Cancer (Cancer #1)

2009-06-10T03:47:00.002-07:00

How cancer develops

2009-06-10T03:47:00.001-07:00

3D Medical Animation - What is Cancer?

2009-06-10T03:46:00.001-07:00

Defence cancer juice

2009-05-30T17:38:00.001-07:00

The cancer cell

2009-05-18T07:20:00.000-07:00

The characteristics of normal cells
Normal body cells have a number of important characteristics. They can

Reproduce themselves exactly
Stop reproducing at the right time
Stick together in the right place
Self destruct if they are damaged
Become specialised or 'mature'
How cancer cells are different
Cancer cells are different to normal cells in several ways. They don't die if they move to another part of the body and

Cancer cells don't stop reproducing
Cancer cells don't obey signals from other cells
Cancer cells don't stick together
Cancer cells don't specialise, but stay immature
Cancer cells don't stop reproducing
Unlike normal cells, cancer cells do not stop reproducing after they have doubled 50 or 60 times. This means that a cancer cell will go on and on and on doubling. So one cell becomes 2, then 4, then 8, then 16....

The cancer cells may be able to stop themselves self destructing. Or they may self destruct more slowly than they reproduce, so that their numbers continue to increase. Eventually a tumour is formed that is made up of billions of copies of the original cancerous cell. Scientists describe cancer cells as being 'immortal'.

Cancer cells don't obey signals from other cells
Something in the cancer cells overrides the normal signalling system. This may be because the genes that tell the cell to reproduce keep on and on firing. Or because the genes that normally tell the cell to stop reproducing have been damaged or lost. So the cancer cell keeps on doubling, regardless of the damage the extra cells cause to the part of the body where the cancer is growing.

Cancer cells don't stick together
Cancer cells can lose the molecules on their surface that keep normal cells in the right place. So they can become detached from their neighbours.

Cancer cells don't specialise, but stay immature
Unlike normal cells, cancer cells do not carry on maturing once they have been made. In fact, the cells in a cancer can become even less mature over time. With all the reproducing, it is not surprising that more of the genetic information in the cell can become lost. So the cells become more and more primitive and tend to reproduce more quickly and even more haphazardly.

Grade and cancer cells
You may hear your doctor talk about the 'grade' of your cancer. This means how well developed or mature the cells look under a microscope. The more the cancer cells look like a normal cell, the more they will behave like one

The more normal a cancer cell looks, the lower its grade
The more abnormal or less well developed a cancer cell is, the higher its grade
Doctors call this 'differentiation'. Cells can be well differentiated, moderately differentiated, or poorly differentiated. This is the same as low, medium or high grade. It is also called grades 1, 2, or 3, where grade 1 is low grade.

Although there are many different ways of talking about this, it all comes down to the same thing. A low grade cancer is likely to grow more slowly and be less likely to spread than a high grade one. Doctors cannot be certain exactly how the cells will behave. But grade is a useful indicator. Grade is one of the factors doctors use to decide on treatment with some types of cancer.
Information about cancer cell more

Cancer Control in Thailand

2009-05-04T04:28:00.000-07:00

ABSTRACT

Cancer in Thailand is becoming a significant health problem. It is the leading cause of death in Thailand. Several cancers can be prevented by a nationwide campaign of health education to prevent raw fish intake and an antismoking campaign. An appropriate cervical cancer and breast cancer screening program can improve the recent prevalence of both and lead to better results of treatment. Research related to the carcinogenesis mechanism of certain cancers can lead to greater understanding and a better plan of control.

INTRODUCTION

Cancer has been the leading cause of death in Thailand with the age-adjusted mortality rate from the two cancer registries being 89.7 per 100 000 in males, 67.2 per 100 000 in females in Khon Kaen and 133.3 in males, 121.0 in females in Chiang Mai (1,2). The estimated age-adjusted incidence rates of cancer for all sites in Thailand were 150.4 per 100 000 for males and 123.0 for females (3), which are not that significant when compared with earlier data (149.6 for males and 125.2 for females) (4). The incidence rates are comparable to those in Asian countries but about half of those in Western countries

Cancer Genetics Overview

2009-04-25T02:47:00.000-07:00

The etiology of cancer is multifactorial, with genetic, environmental, medical, and lifestyle factors interacting to produce a given malignancy. Knowledge of cancer genetics is rapidly improving our understanding of cancer biology, helping to identify at-risk individuals, furthering the ability to characterize malignancies, establishing treatment tailored to the molecular fingerprint of the disease, and leading to the development of new therapeutic modalities. As a consequence, this expanding knowledge base has implications for all aspects of cancer management, including prevention, screening, and treatment.

Genetic information provides a means to identify people who have an increased risk of cancer. Sources of genetic information include biologic samples of DNA, information derived from a person’s family history of disease, findings from physical examinations, and medical records. DNA-based information can be gathered, stored, and analyzed at any time during an individual’s life span, from before conception to after death. Family history may identify people with a modest to moderately increased risk of cancer or may serve as the first step in the identification of an inherited cancer predisposition that confers a very high lifetime risk of cancer. For an increasing number of diseases, DNA-based testing can be used to identify a specific mutation as the cause of inherited risk and to determine whether family members have inherited the disease-related mutation.

Throughout this summary, the term “mutation” will be used to refer to a change in the usual DNA sequence of a particular gene. Mutations can have harmful, beneficial, neutral, or uncertain effects on health and may be inherited as autosomal dominant, autosomal recessive, or X-linked traits. Mutations that cause serious disability early in life are usually rare because of their adverse effect on life expectancy and reproduction. However, if the mutation is autosomal recessive—that is, if the health effect of the mutation is caused only when two copies (one from each parent) of the mutated gene are inherited—mutation carriers (healthy people carrying one copy of the altered gene) may be relatively common in the general population. "Common" in this context refers, by convention, to a prevalence of 1% or more. Mutations that cause health effects in middle and older age, including several mutations known to cause a predisposition to cancer, may also be relatively common. Many cancer-predisposing traits are inherited in an autosomal dominant fashion, that is, the cancer susceptibility occurs when only one copy of the altered gene is inherited. For autosomal dominant conditions, the term “carrier” is often used in a less formal manner to denote people who have inherited the genetic predisposition conferred by the mutation. Refer to individual PDQ summaries focused on the genetics of specific cancers for detailed information on known cancer-susceptibility syndromes.

Increasingly, the public is turning to the Internet for information related both to familial and genetic susceptibility to cancer and to genetic risk assessment and testing. Direct-to-consumer marketing of genetic testing for hereditary breast and colon cancer is also taking place in some communities. This wider availability of information related to inherited cancer risk may raise concerns among persons previously unaware of the implications inherent in their family histories and may lead some of these individuals to consult their primary care physicians for management advice and recommendations. In many instances, the evaluation and advice will be relatively straightforward for physicians with a basic knowledge of familial cancer. In a subset of patients, the evaluation may be more complex, calling for referral to genetics professionals for further evaluation and counseling.

Correctly recognizing and identifying individuals and families at increased risk of developing cancer is one of countless important roles for primary care and other health care providers. Once identified, these individuals can then be appropriately referred for genetic counseling, risk assessment, consideration of genetic testing, and development of a management plan. When medical and family histories reveal cardinal clues to the presence of an underlying familial or genetic cancer susceptibility disorder (see list below),[1] further evaluation may be warranted. Refer to the PDQ summary on Cancer Genetics Risk Assessment and Counseling for more information about the components of a genetics cancer risk assessment.

Features of hereditary cancer include the following:

In the individual patient:
Multiple primary tumors in the same organ.
Multiple primary tumors in different organs.
Bilateral primary tumors in paired organs.
Multifocality within a single organ (e.g., multiple tumors in the same breast all of which have risen from one original tumor).
Younger-than-usual age at tumor diagnosis.
Tumors with rare histology.
Tumors occurring in the sex not usually affected (e.g., breast cancer in men).
Tumors associated with other genetic traits.
Tumors associated with congenital defects.
Tumors associated with an inherited precursor lesion.
Tumors associated with another rare disease.
Tumors associated with cutaneous lesions known to be related to cancer susceptibility disorders (e.g., the genodermatoses).
In the patient’s family:
One first-degree relative with the same or a related tumor and one of the individual features listed.
Two or more first-degree relatives with tumors of the same site.
Two or more first-degree relatives with tumor types belonging to a known familial cancer syndrome.
Two or more first-degree relatives with rare tumors.
Three or more relatives in two generations with tumors of the same site or etiologically related sites.
Concluding that an individual is at increased risk of developing cancer may have important, potentially life-saving management implications and may lead to specific interventions aimed at reducing risk (e.g., tamoxifen for breast cancer, colonoscopy for colon cancer, or risk-reducing salpingo-oophorectomy for ovarian cancer). Information about familial cancer risk may also inform a person’s ability to plan for the future (lifestyle and health care decisions, family planning, or other decisions). Genetic information may also provide a direct health benefit by demonstrating the lack of an inherited cancer susceptibility. For example, if a family is known to carry a cancer-predisposing mutation in a particular gene, a family member may experience reduced worry and lower health care costs if his or her genetic test indicates that he or she does not carry the family’s disease-related mutation. Conversely, information about familial cancer risk may have psychological effects or social costs (e.g., worry, guilt, or increased health care costs). Family dynamics also may be affected. For instance, the involvement of one or more family members may be required for genetic testing to be informative, and parents may feel guilt about passing inherited risk on to their children.

Knowledge about a cancer-predisposing mutation can be informative not only for the individual tested but also for other family members. Family members who previously had not considered the implications of their family history for their own health may be led to do so, and some will undergo genetic testing, resulting in more definitive information on whether they are at increased genetic risk. Some relatives may learn their mutation status without being directly tested, for example, when a biological parent of a child who is a known mutation carrier is identified as an obligate carrier. Founder effects may result in the recognition that specific ethnic groups have a higher prevalence of certain mutations, knowledge that can be both clinically useful (permitting more rational genetic testing strategies) or potentially stigmatizing. Testing may reveal the presence of nonpaternity in a family. There is the theoretical possibility that genetic information may be misused, and concerns about the potential for insurance and/or employment discrimination may arise. Genetic information may also affect medical and lifestyle decisions

Thyroid cancer

2009-04-25T02:41:00.000-07:00

Definition of thyroid cancer: Cancer that forms in the thyroid gland (an organ at the base of the throat that makes hormones that help control heart rate, blood pressure, body temperature, and weight). Four main types of thyroid cancer are papillary, follicular, medullary, and anaplastic thyroid cancer. The four types are based on how the cancer cells look under a microscope.

Family history and other risk factors for medullary thyroid cancer
Major genes associated with medullary thyroid cancer risk
Genetic testing, screening and risk modification for hereditary medullary thyroid cancer
Psychosocial issues associated with hereditary medullary thyroid cancer and genetic testing
The summary also contains level-of-evidence designations. These designations are intended to help readers assess the strength of the evidence in relation to specific studies or strategies. A description of how level-of-evidence designations are made is described in detail in the PDQ summary Cancer Genetics Overview.

This summary is intended to provide clinicians a framework for discussing genetic testing, screening, and risk modification options with individuals at risk for medullary thyroid cancer, as well as for making referrals to cancer risk counseling services. It does not provide formal guidelines or recommendations for making health care decisions. Information in this summary should not be used as a basis for reimbursement determinations.

Vitamin D and Cancer Prevention

2009-04-22T05:51:00.000-07:00

Skin Cancer/Sunscreen - the Dilemma

2009-04-22T05:49:00.000-07:00

Melatonin and breast cancer

2009-04-12T18:14:00.001-07:00

Melatonin has been shown in previous studies to prevent the growth and multiplication on estrogen-responsive MCF-7 cells. A MCF-7 cell is a type of breast cancer cell that is frequently studied in laboratories in order to evaluate the benefits of different chemotherapeutic agents. The purpose of the current trial was to investigate the effects of melatonin on the invasion capacity of MCF-7 cells. When cancer cells grow, they have the capacity to invade other tissues and spread.
In vitro, when melatonin at physiological doses was added to MCF-7 cells, it reduced the invasiveness of these tumor cells. Physiological doses are equivalent to the amount normally found in the body when melatonin is released at night from the pineal gland. Melatonin reduced the invasiveness of MCF-7 cells by causing a decrease in cell attachment and cell motility, and probably by interacting with the estrogen-mediated mechanisms of MCF-7 cell invasiveness. These may, in part, account for melatonin's cancer-stopping action in laboratory studies.

Comments: For the past decade, many researchers, particularly in Italy, have been testing the role of melatonin in the therapy of various cancers. The early research looks promising and some of the studies have shown this hormone to slow the progression of certain cancers. Most of the time, the dosages used for therapy have ranged in the 3 to 20 mg range. If you have breast cancer, you may wish to discuss with your health care practitioner or oncologist whether adding melatonin may be an additional therapeutic option.

Cos S, Fernandez R, Guezmes A, Sanchez-Barcelo EJ. Influence of melatonin on invasive and metastatic properties of MCF-7 human breast cancer cells.Cancer Res 1998 Oct 1;58(19):4383-90

Understanding Cancer

2009-04-09T05:39:00.000-07:00

Cancer begins in cells, the building blocks that form tissues. Tissues make up the organs of the body.

Normally, cells grow and divide to form new cells as the body needs them. When cells grow old, they die, and new cells take their place.

Sometimes, this orderly process goes wrong. New cells form when the body does not need them, and old cells do not die when they should. These extra cells can form a mass of tissue called a growth or tumor.

Tumors can be benign or malignant:

Benign tumors are not cancer:
Benign tumors are rarely life-threatening.
Generally, benign tumors can be removed, and they usually do not grow back.
Cells from benign tumors do not invade the tissues around them.
Cells from benign tumors do not spread to other parts of the body.
Malignant tumors are cancer:
Malignant tumors are generally more serious than benign tumors. They may be life-threatening.
Malignant tumors often can be removed, but sometimes they grow back.
Cells from malignant tumors can invade and damage nearby tissues and organs.
Cells from malignant tumors can spread (metastasize) to other parts of the body. Cancer cells spread by breaking away from the original (primary) tumor and entering the bloodstream or lymphatic system. The cells can invade other organs, forming new tumors that damage these organs. The spread of cancer is called metastasis.
Most cancers are named for where they start. For example, lung cancer starts in the lung, and breast cancer starts in the breast. Lymphoma is cancer that starts in the lymphatic system. And leukemia is cancer that starts in white blood cells (leukocytes).

When cancer spreads and forms a new tumor in another part of the body, the new tumor has the same kind of abnormal cells and the same name as the primary tumor. For example, if prostate cancer spreads to the bones, the cancer cells in the bones are actually prostate cancer cells. The disease is metastatic prostate cancer, not bone cancer. For that reason, it is treated as prostate cancer, not bone cancer. Doctors sometimes call the new tumor "distant" or metastatic disease.

Breast Cancer Risk and Risk Factors

2009-03-31T16:23:00.001-07:00

By now you may be familiar with the statistic that says 1 in 8 women will develop breast cancer. Many people misinterpret this to mean that, on any given day, they and the women they know have a 1-in-8 risk of developing the disease. That’s simply not true.

In reality, about 1 in 8 women in the United States — or 13%, or 13 out of every 100 — can expect to develop breast cancer over the course of an entire lifetime. In the U.S., an average lifetime is about 80 years. So, it’s more accurate to say that 1 in 8 women in the U.S. who reach the age of 80 can expect to develop breast cancer. In each decade of life, the risk of getting breast cancer is actually lower than 13% for most women.

People tend to have very different ways of viewing risk. For you, a 1-in-8 lifetime risk may seem like a high likelihood of getting breast cancer. Or you may turn this around and reason that there is a 7-in-8, or 87.5%, chance you will never get breast cancer, even if you live to age 80. How you view risk often depends on your individual situation — for example, whether you or many women you know have had breast cancer, or you have reason to believe you are at higher-than-normal risk for the disease — and your usual way of looking at the world.

Even though studies have found that women have a 13% lifetime risk of developing breast cancer, your individual risk may be higher or lower than that. Individual risk is affected by many different factors, such as family history, reproductive history, lifestyle, environment, and others.

This section is designed to help you better understand breast cancer risk and some of the factors that can increase risk.

What Is Breast Cancer

2009-03-31T16:21:00.000-07:00

Breast cancer is an uncontrolled growth of breast cells. To better understand breast cancer, it helps to understand how any cancer can develop.

Cancer occurs as a result of mutations, or abnormal changes, in the genes responsible for regulating the growth of cells and keeping them healthy. The genes are in each cell’s nucleus, which acts as the “control room” of each cell. Normally, the cells in our bodies replace themselves through an orderly process of cell growth: healthy new cells take over as old ones die out. But over time, mutations can “turn on” certain genes and “turn off” others in a cell. That changed cell gains the ability to keep dividing without control or order, producing more cells just like it and forming a tumor.

A tumor can be benign (not dangerous to health) or malignant (has the potential to be dangerous). Benign tumors are not considered cancerous: their cells are close to normal in appearance, they grow slowly, and they do not invade nearby tissues or spread to other parts of the body. Malignant tumors are cancerous. Left unchecked, malignant cells eventually can spread beyond the original tumor to other parts of the body.

The term “breast cancer” refers to a malignant tumor that has developed from cells in the breast. Usually breast cancer either begins in the cells of the lobules, which are the milk-producing glands, or the ducts, the passages that drain milk from the lobules to the nipple. Less commonly, breast cancer can begin in the stromal tissues, which include the fatty and fibrous connective tissues of the breast.

Over time, cancer cells can invade nearby healthy breast tissue and make their way into the underarm lymph nodes, small organs that filter out foreign substances in the body. If cancer cells get into the lymph nodes, they then have a pathway into other parts of the body. The breast cancer’s stage refers to how far the cancer cells have spread beyond the original tumor (see Stages of Breast Cancer table for more information).

Breast cancer is always caused by a genetic abnormality (a “mistake” in the genetic material). However, only 5-10% of cancers are due to an abnormality inherited from your mother or father. About 90% of breast cancers are due to genetic abnormalities that happen as a result of the aging process and the “wear and tear” of life in general.

While there are steps every person can take to help the body stay as healthy as possible (such as eating a balanced diet, not smoking, limiting alcohol, and exercising regularly), breast cancer is never anyone's fault. Feeling guilty, or telling yourself that breast cancer happened because of something you or anyone else did, is not productive.

Symptoms of Breast Cancer

2009-03-31T16:19:00.000-07:00

Initially, breast cancer may not cause any symptoms. A lump may be too small for you to feel or to cause any unusual changes you can notice on your own. Often, an abnormal area turns up on a screening mammogram (x-ray of the breast), which leads to further testing.

In some cases, however, the first sign of breast cancer is a new lump or mass in the breast that you or your doctor can feel. A lump that is painless, hard, and has uneven edges is more likely to be cancer. But sometimes cancers can be tender, soft, and rounded. So it's important to have anything unusual checked by your doctor.

According to the American Cancer Society, any of the following unusual changes in the breast can be a symptom of breast cancer:

-swelling of all or part of the breast
-skin irritation or dimpling
-breast pain
-nipple pain or the nipple turning inward
-redness, scaliness, or thickening of the nipple or breast skin
-a nipple discharge other than breast milk
-a lump in the underarm area

These changes also can be signs of less serious conditions that are not cancerous, such as an infection or a cyst. It’s important to get any breast changes checked out promptly by a doctor.

checking for cancer

2009-03-30T08:26:00.001-07:00

Early gastric cancer

2009-03-11T17:56:00.001-07:00

CANCER RECTUM

2009-03-11T17:54:00.001-07:00

Colon cancer symptoms and information

2009-03-11T17:52:00.000-07:00

Shotgun Histology Lymph Node

2009-02-24T16:17:00.001-08:00

Shotgun Histology Pancreas

2009-02-15T07:40:00.000-08:00

Food Fitness and Prostate Cancer

2009-02-05T10:08:00.000-08:00

Cancer Cure: The One-Minute Cure for Cancer & Other Diseases

2009-02-02T00:54:00.001-08:00

Cancer Research: Winning Results With Super Green Drink Diet

2009-02-02T00:52:00.000-08:00

Amazing Healing 8 : Cancer Of The Lips & Vagina

2009-02-01T07:33:00.000-08:00

Colon Cancer

2009-02-01T07:31:00.000-08:00

Shotgun Histology Colon

2009-01-30T00:56:00.002-08:00

Histopathology Colon --Pseudomembranous colitis

2009-01-30T00:56:00.001-08:00

Running Raw: Green Smoothies - Tips & Techniques

2009-01-17T11:43:00.000-08:00

Chlorella as a powerful defense against cancer

2009-01-14T03:28:00.000-08:00

Amazing things truly do come in small packages. One of your most powerful weapons against cancer is chlorella -- a unicellular, green algae. This tiny algae packs a powerful punch. In Prescription for Dietary Wellness, Phyllis A. Balch explains, "Chlorella…contains the highest chlorophyll level per ounce of any plant, as well as protein (nearly 58 percent), carbohydrates, all of the B vitamins, vitamins C and E, amino acids (including all nine essential ones), enzymes and rare trace minerals." Due to its dense and nutrient-rich nature, chlorella offers your body a two-fold attack against cancer. You can access these benefits by taking only one or two teaspoons of chlorella once or twice daily, according to Michael Tierra's Treating Cancer with Herbs.
To grasp chlorella's benefits in fighting cancer, you must first understand cancer's connection to immune system dysfunction. Cancer cells develop in all of our bodies, even in those of us who have never "had cancer." When these cancer cells develop, our immune systems naturally and efficiently destroy them before cancer symptoms appear. On the other hand, when cancer symptoms do appear, these symptoms are an indication of the immune system's sudden inability to effectively fight cancer cells that had been appearing all along. In this sense, cancer is an immune system malfunction more than anything else. You can find in-depth information about the cancer/immune system link on News Target's Cancer page.

With that in mind, one of your best defenses against cancer is to strengthen your immune system. This is where chlorella comes in. Although Western medicine has largely ignored chlorella, Japanese scientists have been widely researching chlorella's benefits since the atomic bombings of Hiroshima and Nagasaki. As Dr. Ralph W. Moss describes in Cancer Therapy, "Japanese scientists studied Chlorella pyrenoidosa as a biological response modifier … Since chlorella does not directly kill cancer cells, the scientists concluded that its effects were caused by boosting the immune response."

In one Japanese study, scientists placed lab mice on a chlorella regimen for ten days, then injected the mice with three types of cancer. According to Dr. Moss, over 70 percent of the chlorella-strengthened mice did not develop cancer, while all of the untreated mice died within 20 days.

Research regarding chlorella's immune-boosting effect is not limited to animal studies. According to Herbal Medicine, Healing Cancer by Dr. Donald R. Yance, Jr., a Virginia-based study treated 15 glioblastoma patients with powdered and liquid chlorella combined at times with standard chemotherapy and/or radiation therapy. Although glioblastoma patients normally display a two-year survival rate of 10 percent, the 15 chlorella-treated patients exhibited a survival rate of 40 percent.

This is only one of the many successful studies linking chlorella to strengthened immune response, thus making chlorella a necessary component of effective and well-rounded cancer treatment. In Treating Cancer with Herbs, Michael Tierra, ND, writes, "I recommend chlorella to all cancer patients regardless of any other green drink they might use … It is virtually a complete food in itself. It acts as both a powerful nutrient and a detoxifying food."

In addition to strengthening the immune system's response to cancer cells, the mighty chlorella acts as a preventative measure against cancer by raising blood levels of the protein albumin. According to Earl Mindell's Supplement Bible, by Earl Mindell, RPh, PhD, "Numerous studies have documented that a low albumin level is a marker for serious illnesses such as cancer and heart disease. They point to test-tube studies confirming that raising albumin levels can both prevent cancerous changes and extend the life span of human cells."

If you have already developed cancer, we urge you to talk with your heath care provider, preferably a naturopath, about adding chlorella to your diet. If you are cancer-free, chlorella can potentially help prevent you from developing cancer. According to natural healers everywhere, chlorella can also reduce fatigue, making you feel both stronger and healthier. This single-celled algae is a small, but mighty, weapon against disease.

Patrick Swayze on His Cancer Battle

2009-01-08T14:55:00.000-08:00

2009-01-05T07:00:00.000-08:00

Leukemia is cancer that starts in the tissue that forms blood. To understand cancer, it helps to know how normal blood cells form.

Normal Blood Cells

Most blood cells develop from cells in the bone marrow called stem cells. Bone marrow is the soft material in the center of most bones.

Stem cells mature into different kinds of blood cells. Each kind has a special job:

White blood cells help fight infection. There are several types of white blood cells.
Red blood cells carry oxygen to tissues throughout the body.
Platelets help form blood clots that control bleeding.

White blood cells, red blood cells, and platelets are made from stem cells as the body needs them. When cells grow old or get damaged, they die, and new cells take their place.

The picture below shows how stem cells can mature into different types of white blood cells. First, a stem cell matures into either a myeloid stem cell or a lymphoid stem cell:

A myeloid stem cell matures into a myeloid blast. The blast can form a red blood cell, platelets, or one of several types of white blood cells.

A lymphoid stem cell matures into a lymphoid blast. The blast can form one of several types of white blood cells, such as B cells or T cells.
The white blood cells that form from myeloid blasts are different from the white blood cells that form from lymphoid blasts.

Picture of blood cells maturing from stem cells.

Most blood cells mature in the bone marrow and then move into the blood vessels. Blood flowing through the blood vessels and heart is called the peripheral blood.

Leukemia Cells

In a person with leukemia, the bone marrow makes abnormal white blood cells. The abnormal cells are leukemia cells.

Unlike normal blood cells, leukemia cells don't die when they should. They may crowd out normal white blood cells, red blood cells, and platelets. This makes it hard for normal blood cells to do their work.

Types of Leukemia

The types of leukemia can be grouped based on how quickly the disease develops and gets worse. Leukemia is either chronic (which usually gets worse slowly) or acute (which usually gets worse quickly):

Chronic leukemia: Early in the disease, the leukemia cells can still do some of the work of normal white blood cells. People may not have any symptoms at first. Doctors often find chronic leukemia during a routine checkup - before there are any symptoms.

Slowly, chronic leukemia gets worse. As the number of leukemia cells in the blood increases, people get symptoms, such as swollen lymph nodes or infections. When symptoms do appear, they are usually mild at first and get worse gradually.

Acute leukemia: The leukemia cells can't do any of the work of normal white blood cells. The number of leukemia cells increases rapidly. Acute leukemia usually worsens quickly.
The types of leukemia also can be grouped based on the type of white blood cell that is affected. Leukemia can start in lymphoid cells or myeloid cells. See the picture of these cells. Leukemia that affects lymphoid cells is called lymphoid, lymphocytic, or lymphoblastic leukemia. Leukemia that affects myeloid cells is called myeloid, myelogenous, or myeloblastic leukemia.

There are four common types of leukemia:

Chronic lymphocytic leukemia (CLL): CLL affects lymphoid cells and usually grows slowly. It accounts for more than 15,000 new cases of leukemia each year. Most often, people diagnosed with the disease are over age 55. It almost never affects children.

Chronic myeloid leukemia (CML): CML affects myeloid cells and usually grows slowly at first. It accounts for nearly 5,000 new cases of leukemia each year. It mainly affects adults.

Acute lymphocytic (lymphoblastic) leukemia (ALL): ALL affects lymphoid cells and grows quickly. It accounts for more than 5,000 new cases of leukemia each year. ALL is the most common type of leukemia in young children. It also affects adults.

Acute myeloid leukemia (AML): AML affects myeloid cells and grows quickly. It accounts for more than 13,000 new cases of leukemia each year. It occurs in both adults and children.
Hairy cell leukemia is a rare type of chronic leukemia. This booklet is not about hairy cell leukemia or other rare types of leukemia. Together, these rare leukemias account for fewer than 6,000 new cases of leukemia each year. The Cancer Information Service (1-800-4-CANCER) can provide information about rare types of leukemia.

Pancreatic Cancer

2009-01-03T03:30:00.000-08:00

The pancreas is an organ in the upper abdomen located beneath the stomach and adjacent to the first portion of the small intestine, called the duodenum. The pancreas is composed of glands that are responsible for a wide variety of tasks. The glandular functions of the pancreas can be divided into the following 2 categories:

Exocrine: The exocrine glands secrete enzymes into ducts that eventually empty into the duodenum. These enzymes then help in the digestion of food as it moves through the intestines.

Endocrine: The endocrine glands secrete hormones, including insulin, into the bloodstream. Insulin is carried by the blood throughout the rest of the body to assist in the process of using sugar as an energy source. Insulin also controls the levels of sugar in the blood.
The pancreas can be divided into the following 4 anatomical sections:

Head - The rightmost portion that lies adjacent to the duodenum

Uncinate process - An extension of the head of the pancreas

Body - The middle portion of the pancreas

Tail - The leftmost portion of the pancreas that lies adjacent to the spleen
Intraductal papillary mucinous neoplasia (IPMN) is a type of pancreatic cancer that is beginning to be recognized more frequently. This pancreatic cancer has a better prognosis than other types of pancreatic cancer. Intraductal papillary mucinous neoplasia is usually diagnosed endoscopically (see Exams and Tests).

The most common type of pancreatic cancer arises from the exocrine glands and is called adenocarcinoma of the pancreas. The endocrine glands of the pancreas can give rise to a completely different type of cancer, referred to as pancreatic neuroendocrine carcinoma or islet cell tumor. This article only discusses issues related to the more common type of pancreatic adenocarcinoma.

Pancreatic adenocarcinoma is among the most aggressive of all cancers. By the time that pancreatic cancer is diagnosed, most people already have disease that has spread to distant sites in the body. Pancreatic cancer is also relatively resistant to medical treatment, and the only potentially curative treatment is surgery. In 2004, approximately 31,800 people in the United States were diagnosed with pancreatic cancer, and approximately 31,200 people died of this disease. These numbers reflect the challenge in treating pancreatic cancer and the relative lack of curative options.

Inflammatory Breast Cancer

2008-12-24T07:26:00.000-08:00

Oxygen, Ozone Therapy, Cancer Treatment

2008-12-21T21:58:00.001-08:00

Uterine Cancer

2008-12-16T05:32:00.000-08:00

Cancer is a disease in which cells in the body grow out of control. Cancer is always named for the part of the body where it starts, even if it spreads to other body parts later. When cancer starts in the uterus, it is called uterine cancer. The uterus is the pear-shaped organ in a woman's pelvis (the area below your stomach and in between your hip bones). The uterus, also called the womb, is where the baby grows when a woman is pregnant. The most common type of uterine cancer is also called endometrial cancer because it forms in the lining of your uterus, called the endometrium.

When uterine cancer is found early, treatment is most effective. The most common sign of uterine cancer is bleeding that is not normal for you because of when it happens or how heavy it is. This could mean bleeding, even a little bit, after you have gone through menopause; periods that are longer than seven days; bleeding between periods; or any other bleeding that is longer or heavier than is normal for you.

Other symptoms, such as pain or pressure in your pelvis, also may occur if you have uterine cancer. If you have any of these symptoms, talk to your doctor, nurse, or other health care professional right away. They may be caused by something other than cancer, but the only way to know is to see your health care professional.

Cervical Cancer

2008-12-16T05:29:00.000-08:00

Cancer is a disease in which cells in the body grow out of control. Cancer is always named for the part of the body where it starts, even if it spreads to other body parts later. When cancer starts in the cervix, it is called cervical cancer. The cervix is the lower, narrow end of the uterus. Also known as the womb, the uterus is where a baby grows when a woman is pregnant. The cervix connects the upper part of the uterus to the vagina (birth canal).

Cervical cancer is the easiest female cancer to prevent, because there is a vaccine and a screening test available. It also is highly curable when found and treated early.

All women are at risk for cervical cancer. It occurs most often in women aged 30 years and older. In 2004,* 11,892 women in the United States were told they had cervical cancer, and 3,850 died from the disease.† For more information, read HPV-Associated Cervical Cancer Statistics.

It is important to get tested for cervical cancer because 6 of 10 cervical cancers occur in women who have never received a Pap test or have not been tested in the past five years.

The human papillomavirus (HPV), a common virus that can be passed from one person to another during sex, is the main cause of cervical cancer and also causes many vaginal and vulvar cancers. At least half of sexually active people will have HPV at some point in their lives. Keep in mind, many people will have an HPV infection at some time in their lives, but few women will get cervical cancer.

Hairy cell leukemia (HCL)

2008-12-15T05:52:00.002-08:00

Decision to treat
Patients with hairy cell leukemia who are symptom-free typically do not receive immediate treatment. Treatment is generally considered necessary when the patient shows signs and symptoms such as low blood cell counts (e.g., infection-fighting neutrophil count below 1.0 K/µL), frequent infections, unexplained bruises, anemia, or fatigue that is significant enough to disrupt the patient's everyday life.

Typical treatment approach
Patients who need treatment usually receive either one week of cladribine, given daily by intravenous infusion or a simple injection under the skin, or six months of pentostatin, given every four weeks by intravenous infusion. In most cases, one round of treatment will produce a prolonged remission.

Other treatments include rituximab infusion or self-injection with Interferon-alpha. In limited cases, the patient may benefit from splenectomy (removal of the spleen). These treatments are not typically given as the first treatment because their success rates are lower than cladribine or pentostatin.

Chronic myelogenous leukemia (CML)

2008-12-15T05:52:00.001-08:00

There are many possible treatments for CML, but the standard of care for newly diagnosed patients is imatinib (Gleevec) therapy.Compared to most anti-cancer drugs, it has relatively few side effects and can be taken orally at home. With this drug, more than 90% of patients will be able to keep the disease in check for at least five years,[7] so that CML becomes a chronic, manageable condition.

In a more advanced, uncontrolled state, when the patient cannot tolerate imatinib, or if the patient wishes to attempt a permanent cure, then an allogeneic bone marrow transplantation may be performed. This procedure involves high-dose chemotherapy and radiation followed by infusion of bone marrow from a compatible donor. Approximately 30% of patients die from this procedure.

Acute myelogenous leukemia (AML)

2008-12-15T05:51:00.001-08:00

Many different anti-cancer drugs are effective for the treatment of AML. Treatments vary somewhat according to the age of the patient and according to the specific subtype of AML. Overall, the strategy is to control bone marrow and systemic (whole-body) disease, while offering specific treatment for the central nervous system (CNS), if involved.

In general, most oncologists rely on combinations of drugs for the initial, induction phase of chemotherapy. Such combination chemotherapy usually offers the benefits of early remission and a lower risk of disease resistance. Consolidation and maintenance treatments are intended to prevent disease recurrence. Consolidation treatment often entails a repetition of induction chemotherapy or the intensification chemotherapy with additional drugs. By contrast, maintenance treatment involves drug doses that are lower than those administered during the induction phase.

Chronic lymphocytic leukemia (CLL)

2008-12-15T05:50:00.000-08:00

Decision to treat
Hematologists base CLL treatment upon both the stage and symptoms of the individual patient. A large group of CLL patients have low-grade disease, which does not benefit from treatment. Individuals with CLL-related complications or more advanced disease often benefit from treatment. In general, the indications for treatment are:

falling hemoglobin or platelet count
progression to a later stage of disease
painful, disease-related overgrowth of lymph nodes or spleen
an increase in the rate of lymphocyte production
Typical treatment approach
CLL is probably incurable by present treatments. The primary chemotherapeutic plan is combination chemotherapy with chlorambucil or cyclophosphamide, plus a corticosteroid such as prednisone or prednisolone. The use of a corticosteroid has the additional benefit of suppressing some related autoimmune diseases, such as immunohemolytic anemia or immune-mediated thrombocytopenia. In resistant cases, single-agent treatments with nucleoside drugs such as fludarabine, pentostatin, or cladribine may be successful. Younger patients may consider allogeneic or autologous bone marrow transplantation

Treatment

2008-12-15T05:49:00.000-08:00

Acute lymphoblastic leukemia (ALL)

Further information: Acute lymphoblastic leukemia#Treatment
Management of ALL focuses on control of bone marrow and systemic (whole-body) disease. Additionally, treatment must prevent leukemic cells from spreading to other sites, particularly the central nervous system (CNS) e.g. monthly lumbar punctures. In general, ALL treatment is divided into several phases:

Induction chemotherapy to bring about bone marrow remission. For adults, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L-asparaginase or cyclophosphamide. For children with low-risk ALL, standard therapy usually consists of three drugs (prednisone, L-asparaginase, and vincristine) for the first month of treatment.
Consolidation therapy or intensification therapy to eliminate any remaining leukemia cells. There are many different approaches to consolidation, but it is typically a high-dose, multi-drug treatment that is undertaken for a few months. Patients with low- to average-risk ALL receive therapy with antimetabolite drugs such as methotrexate and 6-mercaptopurine (6-MP). High-risk patients receive higher drug doses of these drugs, plus additional drugs.
CNS prophylaxis (preventive therapy) to stop the cancer from spreading to the brain and nervous system in high-risk patients. Standard prophylaxis may include radiation of the head and/or drugs delivered directly into the spine.
Maintenance treatments with chemotherapeutic drugs to prevent disease recurrence once remission has been achieved. Maintenance therapy usually involves lower drug doses, and may continue for up to three years.
Alternatively, allogeneic bone marrow transplantation may be appropriate for high-risk or relapsed patients

Causes and risk factors

2008-12-15T05:40:00.000-08:00

There is no single known cause for all of the different types of leukemia. The different leukemias likely have different causes, and very little is certain about what causes them. Researchers have strong suspicions about four possible causes:

-natural or artificial ionizing radiation
-certain kinds of chemicals
-some viruses
-genetic predispositions

Leukemia, like other cancers, results from somatic mutations in the DNA which activate oncogenes or deactivate tumor suppressor genes, and disrupt the regulation of cell death, differentiation or division. These mutations may occur spontaneously or as a result of exposure to radiation or carcinogenic substances and are likely to be influenced by genetic factors. Cohort and case-control studies have linked exposure to petrochemicals, such as benzene, and hair dyes to the development of some forms of leukemia.

Viruses have also been linked to some forms of leukemia. For example, certain cases of ALL are associated with viral infections by either the human immunodeficiency virus or human T-lymphotropic virus (HTLV-1 and -2, causing adult T-cell leukemia/lymphoma). However, one report suggests exposure to certain germs may offer children limited protection against leukemia.

Fanconi anemia is also a risk factor for developing acute myelogenous leukemia.

Until the cause or causes of leukemia are found, there is no way to prevent the disease. Even when the causes become known, they may not be readily controllable, such as naturally occurring background radiation, and therefore not especially helpful for prevention purposes.

Leukemia:Symptoms

2008-12-15T05:30:00.000-08:00

Damage to the bone marrow, by way of displacing the normal bone marrow cells with higher numbers of immature white blood cells, results in a lack of blood platelets, which are important in the blood clotting process. This means people with leukemia may become bruised, bleed excessively, or develop pinprick bleeds (petechiae).

White blood cells, which are involved in fighting pathogens, may be suppressed or dysfunctional. This could cause the patient's immune system to be unable to fight off a simple infection or to start attacking other body cells. Because leukemia prevents the immune system from working normally, some patients experience frequent infection, ranging from infected tonsils, sores in the mouth, or diarrhea to life-threatening pneumonia or opportunistic infections.

Finally, the red blood cell deficiency leads to anemia, which may cause dyspnea and pallor.

Some patients experience other symptoms. These symptoms might include feeling sick, such as having fevers, chills, night sweats and other flu-like symptoms, or feeling fatigued. Some patients experience nausea or a feeling of fullness due to an enlarged liver and spleen; this can result in unintentional weight loss. If the leukemic cells invade the central nervous system, then neurological symptoms (notably headaches) can occur.

All symptoms associated with leukemia can be attributed to other diseases. Consequently, leukemia is always diagnosed through medical tests.

The word leukemia, which means 'white blood', is derived from the disease's namesake high white blood cell counts that most leukemia patients have before treatment. The high number of white blood cells are apparent when a blood sample is viewed under a microscope. Frequently, these extra white blood cells are immature or dysfunctional. The excessive number of cells can also interfere with the level of other cells, causing a harmful imbalance in the blood count.

Some leukemia patients do not have high white blood cell counts visible during a regular blood count. This less-common condition is called aleukemia. The bone marrow still contains cancerous white blood cells which disrupt the normal production of blood cells. However, the leukemic cells are staying in the marrow instead of entering the bloodstream, where they would be visible in a blood test. For an aleukemic patient, the white blood cell counts in the bloodstream can be normal or low. Aleukemia can occur in any of the four major types of leukemia, and is particularly common in hairy cell leukemia.

Leukemia

2008-12-15T05:02:00.001-08:00

Leukemia or leukaemia (Greek leukos λευκός, "white"; aima αίμα, "blood") is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation (production by multiplication) of blood cells, usually white blood cells (leukocytes). Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases called hematological neoplasms.

Classification

Leukemia is clinically and pathologically subdivided into several large groups. The first division is between its acute and chronic forms:

Acute leukemia is characterized by the rapid increase of immature blood cells. This crowding makes the bone marrow unable to produce healthy blood cells. Immediate treatment is required in acute leukemias due to the rapid progression and accumulation of the malignant cells, which then spill over into the bloodstream and spread to other organs of the body. Acute forms of leukemia are the most common forms of leukemia in children.

Chronic leukemia is distinguished by the excessive build up of relatively mature, but still abnormal, blood cells. Typically taking months or years to progress, the cells are produced at a much higher rate than normal cells, resulting in many abnormal white blood cells in the blood. Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy. Chronic leukemia mostly occurs in older people, but can theoretically occur in any age group.

Additionally, the diseases are subdivided according to which kind of blood cell is affected. This split divides leukemias into lymphoblastic or lymphocytic leukemias and myeloid or myelogenous leukemias:

In lymphoblastic or lymphocytic leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form lymphocytes, which are infection-fighting immune system cells.

In myeloid or myelogenous leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form red blood cells, some other types of white cells, and platelets.

Lymph Nodes Cancer

2008-12-08T11:46:00.000-08:00

Lymph node cancer or lymphoma is a cancer that accounts for approximately five percent of all cancers. It predominantly effects males but is not exclusive to men. Those most at risk are between the ages of fifteen and thirty four and those over the age of fifty-four. This does not mean that anyone outside of this age range is not at risk but statistically it does seem to fall inside those age groups at a greater rate. Like all other cancers, early detection and treatment is the key to a greater chance of recovery.

Hodgkins Disease is a form of lymph node cancer but is rare in its occurrence. It also statistically effects mostly men between the ages of fifteen and thirty-four and men over the age of fifty-four but is not exclusive to men only. Some of the most common symptoms of Hodgkins Disease are night sweats, unexplained wight loss, constant fatigue and unexplained fever. If you are experiencing any or all of these symptoms it is wise to have yourself examined by a doctor as these also could be the symptoms of another disorder.

All other remaining types of lymph node cancer are known as non-Hodgkins lymphoma. The majority of lymph node cancers treated are of the non-Hodgkins type. The symptoms of non-Hodgkins lymphoma are the same as Hodgkins Disease. Night sweats, unexplained fever, chronic fatigue and unexplained weight loss.Lymph node cancer is also known as lymphatic cancer. Those with a family history of lymph node cancer statistically fall within a higher risk group of contracting the disease. This is true for both men and women.

Lymph node cancer is a type of cancer that involves the lymphatic system. The lymphatic system is an integral part of the bodies immune system. Statistically, the occurrence of lymph node cancer has increased approximately seventy-five percent since nineteen-seventy-three in the United States. Research has revealed that approximately one in fifty-two men and one in sixty-one women in the United States will contract non Hodgkin lymphoma within their lifetime. Studies have indicated that a greater exposure to herbicides and pesticides is greatly responsible for this increase.

Lymph node cancer is curable and if detected early and with effective treatment a person with lymph node cancer has a greater chance than ever before of being cured of this disease and if cured can expect to live a long and normal life. Many new and innovative treatments for lymph node cancer have been developed and are now available. The medical community has a greater understanding of lymph node cancer than in years past. Treatments that were once experimental and have been found to be effective are now being used to treat and cure lymph node cancer.

As a person ages it is to be expected that he or she will encounter medical challenges, it is part of the aging process. Lymph node cancer might be one of those challenges you encounter in your life's journey. How soundly these challenges are defeated depends greatly on how you approach them. A fighting spirit has been proven time and again to be a powerful weapon to have in your arsenal when battling cancers of all types. Accepting defeat in any challenge almost guarantees defeat. The will to fight and live on has carried so many cancer survivors to victory over the disease.

Thyroid Cancer

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Testicular Cancer

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Testicular cancer primarily affects men between the ages of 15 and 35. However, men of any age can develop the disease. The good news is that when found early, testicular cancer is almost always treatable

Testicular Cancer - What is Testicular Cancer?
What is testicular cancer? Explore the basics of testicular cancer, including the causes, symptoms, prevention, and treatment of the disease.

Testicular Cancer Prevention
Learn more about testicular cancer prevention.

Testicular Cancer
A look into testicular cancer and it's causes, symptoms, and statistical information.

Symptoms of Testicular Cancer
The symptoms of tsticular cancer are explained here in an in depth FAQ.

Testicular Cancer Causes
A look into the causes of testicular cancer and the risk factors for the disease.

Testicular Cancer Risk Factors
Learn what the risk factors and causes of testicular cancer are in this mini article. Knowing the risk factors of testicular cancer and avoiding them is the first step in preventing the disease.

Types of Testicular Cancer

There are two two types of testicular cancers. Discover the different types and the characteristics of each.

How To Do a Testicluar Self Exam
Learning how to perform a testicular self exam can help detect testicular cancer at its early stages. This simple guide will teach you how, what to look for, and how often to to do the exam.

Cervical Screening (smear testing)

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Skin cancer

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Skin cancer is a malignant growth on the skin which can have many causes. Skin cancer generally develops in the epidermis (the outermost layer of skin), so a tumor is usually clearly visible. This makes most skin cancers detectable in the early stages. There are three common types of skin cancer, each of which is named after the type of skin cell from which it arises. Cancers caused by UV exposure may be prevented by avoiding exposure to sunlight or other UV sources, and wearing sun-protective clothes. The use of sunscreen is recommended by medical organizations as a measure that helps to protect against skin cancer (see sunscreen).

Unlike many other cancers, including those originating in the lung, pancreas, and stomach, only a small minority of those afflicted will actually die of the disease.[citation needed] Skin cancers are the fastest growing type of cancer in the United States. Skin cancer represents the most commonly diagnosed malignancy, surpassing lung, breast, colorectal and prostate cancer. Melanoma is the least common skin cancer but it is potentially the most serious: there are over 8,000 new cases each year in the UK and 1,800 deaths. More people now die of Melanoma in the UK than in Australia. It is the second most common cancer in the young population (20 – 39 age group). It is estimated that approximately 85% of cases are caused by too much sun. Non-melanoma skin cancers are the commonest skin cancers. The majority of these are called Basal Cell Carcinomas. These are usually localised growths caused by excessive cumulative exposure to the sun and do not tend to spread.

Risk factors

Skin cancer is most closely associated with chronic inflammation of the skin. This includes:

Overexposure to UV-radiation can cause skin cancer either via the direct DNA damage or via the indirect DNA damage mechanism. UVA & UVB have both been implicated in causing DNA damage resulting in cancer. Sun exposure between 10AM and 4PM is most intense and therefore most harmful. Natural (sun) & artificial UV exposure (tanning salons) are associated with skin cancer.[citation needed] Since sunbeds cause mostly indirect DNA damage (free radicals) their use is associated with the deadliest form of skin cancer, malignant melanoma.[citation needed]

UVA rays affect the skin at a deeper level than UVB rays, reaching through the epidermis and the dermis to the hypodermis where connective tissues and blood vessels are located. UVA activates the melanin of the epidermis causing changes in pigmentation as well as loss of elasticity of the skin, which contributes to premature wrinkling, sagging and aging of the skin.

UVB rays primarily affect the epidermis causing sunburns, redness, and blistering of the skin. The melanin of the epidermis is activated with UVB just as with UVA; however, the effects are longer lasting with pigmentation continuing over 24 hours.
Chronic non-healing wounds, especially burns. These are called Marjolin's ulcers based on their appearance, and can develop into squamous cell carcinoma.
Genetic predisposition, including "Congenital Melanocytic Nevi Syndrome". CMNS is characterized by the presence of "nevi" or moles of varying size that either appear at or within 6 months of birth. Nevi larger than 20 mm (3/4") in size are at higher risk for becoming cancerous.

Skin cancer is one of the potential dangers of ultraviolet germicidal irradiation.
Many believe that skin cancer can be prevented altogether by avoiding sunlight entirely, or wearing protective clothing while outdoors. However, studies show that Melanoma Skin Cancer is more common in those who work indoors. Skin Cancer is most common on areas of the body that are not normally exposed to the sun, and then exposing the skin to UV rays excessively.

Skin cancer generally has a 20- to 30-year latency period. The rates of skin cancer we are seeing today in older individuals mostly are a function of the ignorant misbehavior of the 1970s and early 1980s. Recall: Society used to view sunburns as an inconvenient right of spring, or as a “precursor” to developing a summer tan. Severe burns were commonplace. Today we know how reckless that approach was, and the incidence rates of skin cancer today in those over 50 years of age reflect that ignorance

The most common types of skin cancer are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) which may be locally disfiguring but are unlikely to metastasize (spread to other parts of the body). The most dangerous type of skin cancer is malignant melanoma. This form of skin cancer is causing the major part of all skin cancer fatalities.

More rare types of skin cancer include:

-Dermatofibrosarcoma protuberans
-Merkel cell carcinoma
-Kaposi's sarcoma

The BCC and the SCC often carry a UV-signature mutation indicating that these cancers are caused by UV-B radiation via the direct DNA damage. However the malignant melanoma is predominantly caused by UV-A radiation via the indirect DNA damage.[citation needed] The indirect DNA damage is caused by free radicals and reactive oxygen species. It has been shown, that the absorption of three sunscreen ingredients into the skin, combined with a 60-minute exposure to UV, leads to an increase of free radicals in the skin.

Skin cancer as a group

Many laymen and even professionals consider the basal cell carcinoma (BCC), the squamous cell carcinoma (SCC) and the malignant melanoma as one group - namely skin cancer. This grouping is problematic for two reasons:

the mechanism that generates the first two forms is different from the mechanism that generates the melanoma. The direct DNA damage is responsible for BCC and SCC while the indirect DNA damage causes melanoma.
the mortality rate of BCC and SCC is around 0.3 causing 2000 deaths per year in the US. In comparison the mortality rate of melanoma is 15-20% and it causes 138001 deaths per year.
Even though it is rare, malignant melanoma is responsible for 75 % of all skin cancer related death cases.

While sunscreen has been shown to protect against BCC and SCC it may not protect against malignant melanoma. When sunscreen penetrates into the skin it generates reactive chemicals. It has been found that sunscreen use is correlated with malignant melanoma.The lab-experiments and the epidemiological studies indicate that sunscreen use causes melanoma

Signs and symptoms

There are a variety of different skin cancer symptoms. These include crabs or changes in the skin that do not heal, ulcers in the skin, discoloration, and changes in existing moles.

Basal cell carcinoma usually looks like a raised, smooth, pearly bump on the sun-exposed skin of the head, neck or shoulders. Sometimes small blood vessels can be seen within the tumor. Crusting and bleeding in the center of the tumor frequently develops. It is often mistaken for a sore that does not heal.
Squamous cell carcinoma is commonly a red, scaling, thickened patch on sun-exposed skin. Ulceration and bleeding may occur. When SCC is not treated, it may develop into a large mass.

Most melanomas are brown to black looking lesions. Signs that might indicate a malignant melanoma include change in size, shape, color or elevation of a mole. The appearance of a new mole during adulthood, or new pain, itching, ulceration or bleeding.

Treatment

Most skin cancers can be treated by removal of the lesion, making sure that the edges (margins) are free of the tumor cells. These excisions provide the best cure for both early and high-risk disease.

For low-risk disease, radiation therapy and cryotherapy (freezing the cancer off) can provide adequate control of the disease; both, however, have lower overall cure rates than surgery.

Mohs' micrographic surgery is a technique used to remove the cancer with the least amount of surrounding tissue and the edges are checked immediately to see if tumor is found. This provides the opportunity to remove the least amount of tissue and provide the best cosmetically favorable results. This is especially important for areas where excess skin is limited, such as the face. Cure rates are equivalent to wide excision. Special training is required to perform this technique.

In the case of disease that has spread (metastasized), further surgical procedures or chemotherapy may be required.

Scientists have recently been conducting experiments on what they have termed "immune- priming". This therapy is still in its infancy but has been shown to effectively attack foreign threats like viruses and also latch onto and attack skin cancers. More recently researchers have focused their efforts on strengthening the body's own naturally produced "helper T cells" that identify and lock onto cancer cells and help guide the killer cells to the cancer. Researchers infused patients with roughly 5 billion of the helper T cells without any harsh drugs or chemotherapy. This type of treatment if shown to be effective has no side effects and could change the way cancer patients are treated.

Reduction of risk

Although it is impossible to completely eliminate the possibility of skin cancer, the risk of developing such a cancer can be reduced significantly with the following steps:

reducing exposure to ultraviolet (UV) radiation, especially in early years
avoiding sunburns (Recent studies have shown that sunscreen does not protect from melanoma.

avoiding sun exposure during the day (usually from 10 AM to 3 PM), when the sun is highest in the sky

wearing protective clothing (long sleeves and hats) when outdoors
using a broad-spectrum sunscreen that blocks both UVA and UVB radiation
use a sun block of about SPF 50

reapply sun block every 2 hours and after swimming
Although it is generally accepted that UV exposure is the greatest risk factor in melanoma development, some sceptics say that there is no proven data that links moderate sun exposure with the appearance of melanoma.

Pathology

Squamous cell carcinoma is a malignant epithelial tumor which originates in epidermis, squamous mucosa or areas of squamous metaplasia.

Macroscopically, the tumor is often elevated, fungating, or may be ulcerated with irregular borders. Microscopically, tumor cells destroy the basement membrane and form sheets or compact masses which invade the subjacent connective tissue (dermis). In well differentiated carcinomas, tumor cells are pleomorphic/atypical, but resembling normal keratinocytes from prickle layer (large, polygonal, with abundant eosinophilic (pink) cytoplasm and central nucleus). Their disposal tends to be similar to that of normal epidermis: immature/basal cells at the periphery, becoming more mature to the centre of the tumor masses. Tumor cells transform into keratinized squamous cells and form round nodules with concentric, laminated layers, called "cell nests" or "epithelial/keratinous pearls". The surrounding stroma is reduced and contains inflammatory infiltrate (lymphocytes). Poorly differentiated squamous carcinomas contain more pleomorphic cells and no keratinization

Read more...

Treatment of Cervical Cancer

2008-11-10T05:54:00.000-08:00

Once it is determined that you have cervical cancer, your doctor should explain the treatment options available to you and recommend the most appropriate option for you. Treatment for cancer of the cervix depends on such factors as the stage of the cancer, the size of the tumor, and the patient's age, overall health, and desire to have children in the future. The following are standard treatments based upon the stage of the cancer.

Stage 0 Cervical Cancer

Stage 0 cervical cancer is sometimes called carcinoma in situ.

Treatment may be one of the following:

Conization
Laser surgery
Loop electrosurgical excision procedure (LEEP)
Cryosurgery
Surgery

Stage I Cervical Cancer

Treatment may be one of the following depending on how deep the tumor cells have invaded into the normal tissue:

For stage IA cancer:

Surgery to remove the cancer, uterus, and cervix (total abdominal hysterectomy) The ovaries may also be taken out (bilateral salpingo-oophorectomy), but are usually not removed in younger women.
Conization
For tumors with deeper invasion (3-5 millimeters): Surgery to remove the cancer, the uterus and cervix, and part of the vagina (radical hysterectomy) along with the lymph nodes in the pelvic area (lymph node dissection)
Internal radiation therapy

For stage IB cancer:

Combination of internal radiation therapy and external radiation therapy
Radical hysterectomy (removal of the cancer, the uterus and cervix, and part of the vagina) and lymph node dissection
Radical hysterectomy (removal of the cancer, the uterus and cervix, and part of the vagina) and lymph node dissection followed by radiation therapy plus chemotherapy
Radiation therapy plus chemotherapy

Stage II Cervical Cancer

Treatment may be one of the following

For stage IIA cancer:

Combination of internal and external radiation therapy
Radical hysterectomy (removal of the cancer, the uterus and cervix, and part of the vagina) and lymph node dissection
Radical hysterectomy (removal of the cancer, the uterus and cervix, and part of the vagina) and lymph node dissection followed by radiation
Radiation therapy plus chemotherapy

For stage IIB cancer:

Internal and external radiation therapy plus chemotherapy

Stage III Cervical Cancer

Treatment may be one of the following:

internal and external radiation therapy plus chemotherapy

Stage IV Cervical Cancer

Treatment may be one of the following:

For stage IVA cancer:

Internal and external radiation therapy plus chemotherapy

For stage IVB cancer:

Radiation therapy to relieve symptoms caused by the cancer
Chemotherapy

Recurrent Cervical Cancer

If the cancer has come back (recurred) in the pelvis, treatment may be one of the following:

Radiation therapy combined with chemotherapy
Chemotherapy to relieve symptoms caused by the cancer

If the cancer has come back outside of the pelvis, a patient may choose to enter a clinical trial of systemic chemotherapy.

Screening for Cervical Cancer

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Screening for cervical cancer is the testing of women for precancerous developments even in the absence of any symptoms. The intended outcome of cervical cancer screening is different from that of screening for other types of cancer: the primary goal of cervical cancer screening is not to find cancer, but to find precancerous lesions. The reason for this is that detection and treatment of precancerous cervical lesions (dysplasia) can actually prevent cervical cancer from ever occurring. Additionally, if cervical cancer is detected while in its earliest in situ stage, the likelihood of survival is almost 100 percent with timely and appropriate treatment and follow-up.

Screening techniques that also include HPV testing may increase the ability to detect abnormal cell changes early, and may also let a woman know whether or not she carries one of the more dangerous viruses, which would increase the need to be extra vigilant about screening.

All women who are 18 or older, or who are sexually active, should receive yearly pelvic examinations and Pap smears. The Pap smears should be done annually for at least three consecutive negative Pap smears in a row. While some physicians perform Pap smears less regularly after three consecutive negative results, the safer course is to continue to perform yearly Pap smears, especially if there are any risk factors present. In addition, if a woman has previously been treated for cervical or endometrial cancer, more frequent Pap smears are recommended; typically, every 3-6 months in the first 3 years after completion of treatment with surgery or radiation therapy.

The Pap Smear

Pap smears are tests performed during the pelvic examination by inserting a speculim into the vagina so that the Cervix can be visualized and a sample of cells can be removed from the outer portion of the cervix using a wooden or plastic spatula. A small brush is then used to take a second sample from the inner part of the cervix. These samples are immediately preserved on glass slides and are then microscopically analyzed for the presence of cancerous or precancerous changes. For women who have undergone a hysterectomy with removal of the cervix, the vaginal cuff is visually inspected and the sample is taken from the vaginal cuff.

If cancerous or precancerous changes are detected, a cancer diagnosis work-up is required to determine the nature of the cancer and whether it has spread.

Cervical Cancer Diagnosis Workup
If a woman has an abnormal Pap smear, it is appropriate to do a workup to determine whether only precancerous changes are present in the cervix, or whether cancer cells are already present. If cancer cells are already present, it must also be determined how much cancer is present and how far the cancerous cells have spread. If the cancer has spread beyond the cervix, it is said to have metastasized.

Staging the Cervical Cancer
The size and spread of the cancer is classified as the stage of the cancer. Knowing the stage of the cancer is important because it is the primary factor in the selection of treatment and in the prognosis for the woman. One or more of the following tests may be necessary to identify the stage of the cancer:

Colposcopy is a procedure that involves the insertion of a viewing scope (the colposcope) into the vagina in order to magnify the region for inspection. Prior to inserting the colposcope, a Schiller test, a rinse of an iodine solution applied with a cotton swab, is administered to turn abnormal cells yellow or white. Small clusters of these abnormal cells can then be removed for biopsy with an Endocervical Curettage.

Endocervical Curettage (ECC) is often performed during the colposcopy. ECC involves the scraping of cells from the inner portion of the cervix. Since it may not be possible to properly view the inner cervix with the colposcope, performing an ECC may be necessary in order to detect certain forms of cervical cancer, such as adenocarcinoma, which grows in the upper portion of the cervix. Together, colposcope and ECC will identify most cervical cancers.

Loop electrocautery excision procedure (LEEP) In this procedure, abnormal or suspicious cervical tissue is removed with a sharp wire loop and the site is cauterized to eliminate remaining abnormal tissue. The area of the cervix containing abnormal cells is known as the transformation zone.

Conization, or a cone biopsy. This procedure uses a scalpel or laser to remove a cone-shaped section of the cervix for biopsy. Conization helps assess how much tissue is diseased. Because it requires removal of part of the cervix, it is generally recommended when other diagnostic tests have revealed cancerous abnormalities, invasive cervical cancer is suspected, and a comprehensive diagnosis is necessary.

Pelvic Ultrasound is an imaging technique that uses sound waves to produce an image that can be used to measure the size and position of the cancer.

CT Scan (or CAT Scan), which stands for computerized axial tomography, uses computerized X-ray pictures to evaluate internal organs of the body. The CT scan is most often used prior to administering radiation therapy (discussed further under cancer treatment) in order to help calculate how much radiation and where exactly in the body the radiation should be delivered by determining the size and position of the cancer.

MRI, which stands for magnetic resonance imaging is a non-invasive procedure that produces a two-dimensional view of organs and structures. The MRI images can be used to identify abnormal nodules in bones and in the lymph nodes, a sign that the cancer may be spreading.

Endoscopy is a procedure that uses a thin flexible tube (called an endoscope) that has a lens or camera at the end and records images of what is seen through the camera on a computer screen, allowing visualization of internal organs, such as the uterus. Biopsy samples are often taken through the endoscope during the procedure.

Laboratory Tests, such as a blood test and a urine test, can be used to check the cells of the blood to determine the level of functioning of the kidneys and liver. X-rays can be used to check the status of the organs, such as the lungs.

The cancer's stage is documented by using a standard system which assigns letters and numbers to indicate the size and spread of the cancer:

Stage 0 or carcinoma in situ

Carcinoma in situ is very early cancer. When discussing stage 0 and carcinoma in situ of the cervix or vagina, the condition is more properly understood as a pre-cancerous problem that has not yet behaved like a cancer. The abnormal cells are found only in the first layer of cells of the primary site and do not invade the deeper tissues.

Stage I
Cancer involves the primary site, but has not spread to nearby tissues.

stage IA:
a very small amount of cancer -- visible under a microscope -- is found deeper in the tissues.

stage IB:
a larger amount of cancer is found in the tissues.

Stage II
Cancer has spread into surrounding structures such as the upper part of the vagina or nearby lymph nodes but is still inside the primary site.

stage IIA:
cancer has spread beyond the primary site but is limited compared to IIB.

stage IIB:
cancer has spread to other tissue around the primary site.

Stage III
Cancer has spread to surrounding structures such as the lower part of the vagina, nearby lymph nodes, the outer layer of the womb, or nearby structures within the pelvic area.

Stage IV
Cancer has spread beyond the pelvic area, to such areas as the bladder, bowel, lungs, liver, or bone.

stage IVA:
cancer has spread to organs close to the pelvic area.

stage IVB:
cancer has spread to distant organs, such as the lungs.

Recurrent
Recurrent disease means that the cancer has come back (recurred) after it has been treated.

Grading the Cervical Cancer
The malignancy (or aggressiveness) of the cervical cancer is documented by assigning a grade to the cancer. The grade assigned to the cancer is based upon the appearance of the cancer cells and how they are arranged together. The grade is generally determined by a microscopic examination of cancerous cells obtained from the cervix by a biopsy.

The cancer's grade is assigned using a standard grading system which assigns cancer cells a score from 1 to 3:

low-grade cancer. This is the least-aggressive type of cancer. Cells from low-grade cervical cancer have an appearance most like normal cells, and tend to be slow-growing. Such cancer cells are called well-differentiated.

intermediate-grade cancer. By the time the cancer has become intermediate-grade, it has turned more aggressive than a low-grade cancer. Intermediate-grade cancer cells have an appearance that is less like normal cells and is often faster growing than low-grade cancer cells. Such cells are called moderately-differentiated.

high-grade level. This is the most aggressive type of cancer. Cells from high-grade cervical cancer are the least like normal cells. They are rapid-growing and highly aggressive, often spreading into the lymph nodes and bone. Such cells are called poorly-differentiated.

The higher the grade of the cancer, the more difficult it is to successfully treat the cancer.

Once the diagnostic workup is completed, a proper treatment plan can be developed.

Cervical Cancer Basics

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Cervical cancer is among the most common cancer in women. Cervical cancer occurs when the cells in the cervix begin to grow and replicate in an abnormal and uncontrolled way. When this happens, the body cannot organize these cells for normal function and the cells form a mass that is called a tumor. Malignant tumors in the cervix can spread to other parts of the body, crowding and destroying normal cells.

Cervical cancer often grows very slowly over a period of years. Before the cancer actually develops, there are early changes that occur in the cells of the cervix. While these abnormal cells (called cervical intra-epithelial neoplasia or CIN) are not in and of themselves cancerous, and many women with these cells do not develop cancer, these cells may lead to cancer. These cells are sometimes referred to as precancerous, meaning that they have the potential to develop into cancer if not treated.

CIN usually results from a viral infection by the human papillomavirus (HPV). HPV is a common virus that is generally sexually transmitted. While there are dozens of HPV type viruses, only a few have been linked to the development of cervical cancer. Even when women have the virus, their immune system generally eliminates it. For women whose immune system does not eliminate the virus, HPV may in time develop into cervical cancer.

All women are potentially at risk of developing cervical cancer at some point in their lifetime. The most common risk factors for cervical cancer include an early age of first intercourse, having multiple sexual partners, and having experienced a weakened immune system. Cervical cancer is most often diagnosed in women in their late 30s. It can, however, be diagnosed in younger as well as older women.

The most common symptoms of cervical cancer include abnormal bleeding, such as between periods or after intercourse. Sometines, there is also a vaginal discharge, and discomfort during intercourse. Women who have had their menopause may experience new bleeding. While these symptoms can be caused by conditions other than cervical cancer, they should raise your doctor's suspicion that you may have cervical cancer.

Lung Cancer

2008-11-05T19:11:00.000-08:00

How To Eat To Prevent Cancer

2008-11-03T16:18:00.000-08:00

Colon cancer

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Gallbladder cancer

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Gallbladder cancer is a relatively uncommon cancer. If it is diagnosed early enough, it can be cured by removing the gallbladder. Most often it is found after symptoms such as abdominal pain and jaundice occur, and it has spread to other organs such as the liver.

It is a rare cancer that is still being studied and thought to be related to gallstones building up, which also can lead to calcification of the gallbladder, a condition known as Porcelain gallbladder. Porcelain gallbladder is also rare. Some studies indicate that people with porcelain gallbladder have a high risk of developing gallbladder cancer, but other studies question this. The outlook is poor for recovery if the cancer is found after symptoms have started to occur

Risk factors

Gender: Approx. twice more common in women than men, mostly between the ages of 50 and 60.
Obesity increases the risk for gallbladder cancer. It is common in North India indigenous peoples of the Americas.
Primary carcinoma is linked to chronic cholecystitis and cholelithiasis.
Alcohol: "…alcohol drinking is a risk factor of gallbladder cancer…"

Signs and Symptoms

Steady pain in the upper right abdomen for around 2 months.
Diarrhea
Burping
Weakness
Loss of appetite
Weight loss
Vomiting
Infection, leading to peritonitis, gangrene, perforation, and or liver abscess
Jaundice, due to obstruction
Early symptoms mimic gallbladder inflammation and gallstones, which must be excluded as the cause. Later, the symptoms may be that of biliary obstruction.

Disease Course

Most tumors are adenocarcinomas, with a small percent being squamous cell carcinomas. The cancer commonly spreads to the liver, pancreas, stomach,and duodenum.

Diagnosis

Incidentally discovered gallbladder cancer (adenocarcinoma) following a cholecystectomy. H&E stain.Early diagnosis is not generally possible. People at high risk, such as women or Native Americans with frequent gallstones, are evaluated closely. Endoscopic ultrasound, transabdominal ultrasound, CT scan, MRI, and MR cholangiopancreatography can be used to diagnose.

Treatment

The most common and most effective treatment is surgical removal of the gallbladder (cholecystectomy) with lymph node dissection. However, with gallbladder cancer's extremely poor prognosis, most will die by one year following the surgery. If surgery is not possible, endoscopic stenting of the biliary tree can reduce jaundice. Chemotherapy and radiation may also be used with surgery. Mutant Adenovirus based treatment is under investigation by several researcher [5][6] and a company has even got license to use a mutant of Adenovirus (Onyx-15) to cure cancer.

Stomach cancer

2008-10-18T02:44:00.000-07:00

Stomach or gastric cancer can develop in any part of the stomach and may spread throughout the stomach and to other organs; particularly the esophagus and the small intestine. Stomach cancer causes nearly one million deaths worldwide per year

Epidemiology

Stomach cancer is the fourth most common cancer worldwide with 930,000 cases diagnosed in 2002.It is a disease with a high death rate (700,000 per year) making it the second most common cause of cancer death worldwide after lung cancer.

It represents roughly 2% (25,500 cases) of all new cancer cases yearly in the United States, but it is much more common in Korea, Japan, Great Britain, South America, and Iceland. It is associated with high salt in the diet, smoking, and low intake of fruits and vegetables. Infection with the bacterium H. pylori is the main risk factor in about 80% or more of gastric cancers.[citation needed] It is more common in men.

Gastric cancer has very high incidence in Korea and Japan. Gastric cancer is the leading cancer type in Korea with 20.8% of malignant neoplasms, the second leading cause of cancer deaths. It is suspected several risk factors are involved including diet, gastritis, intestinal metaplasia and Helicobacter pylori infection. A Korean diet, high in salted, stewed and broiled foods, is thought to be a contributing factor. Ten percent of cases show a genetic component.In Japan and other countries bracken consumption and spores are correlated to stomach cancer incidence.Epidemiologists have yet to fully account for the high rates of gastric cancer as compared to other countries. Gastric cancer shows a male predominance in its incidence as up to 3 males are affected for every female. Estrogen may protect women against the development of this cancer form.

A very small percentage of diffuse-type gastric cancers (see Histopathology below) are thought to be genetic. Hereditary Diffuse Gastric Cancer (HDGC) has recently been identified and research is ongoing. However, genetic testing and treatment options are already available for families at risk.

Metastasis occurs in 80-90% of individuals with stomach cancer, with a five year survival rate of 75% in those diagnosed in early stages and less than 30% of those diagnosed in late stages.

Symptoms

Stomach cancer is often asymptomatic or causes only nonspecific symptoms in its early stages. By the time symptoms occur, the cancer has generally metastasized to other parts of the body, one of the main reasons for its poor prognosis. Stomach cancer can cause the following signs and symptoms:

Early

Indigestion or a burning sensation (heartburn)
Loss of appetite, especially for meat
Late

Abdominal pain or discomfort in the upper abdomen
Nausea and vomiting
Diarrhea or constipation
Bloating of the stomach after meals
Weight loss
Weakness and fatigue
Bleeding (vomiting blood or having blood in the stool), which can lead to anemia
Dysphagia; this feature suggests a tumor in the cardia or extension of the gastric tumor in to the Oesopagus.
These can be symptoms of other problems such as a stomach virus, gastric ulcer or tropical sprue and diagnosis should be done by a gastroenterologist or an oncologist.

Diagnosis

To find the cause of symptoms, the doctor asks about the patient's medical history, does a physical exam, and may order laboratory studies. The patient may also have one or all of the following exams:

Gastroscopic exam is the diagnostic method of choice. This involves insertion of a fibre optic camera into the stomach to visualize it.
Upper GI series (may be called barium roentgenogram)
Computed tomography or CT scanning of the abdomen may reveal gastric cancer, but is more useful to determine invasion into adjacent tissues, or the presence of spread to local lymph nodes.
Abnormal tissue seen in a gastroscope examination will be biopsied by the surgeon or gastroenterologist. This tissue is then sent to a pathologist for histological examination under a microscope to check for the presence of cancerous cells. A biopsy, with subsequent histological analysis, is the only sure way to confirm the presence of cancer cells.

Various gastroscopic modalities have been developed to increased yield of detect mucosa with a dye that accentuates the cell structure and can identify areas of dysplasia. Endocytoscopy involves ultra-high magnification to visualize cellular structure to better determine areas of dysplasia. Other gastroscopic modalities such as optical coherence tomography are also being tested investigationally for similar applications.

A number of cutaneous conditions are associated with gastric cancer. A condition of darkened hyperplasia of the skin, frequently of the axilla and groin, known as acanthosis nigricans, is associated with intra-abdominal cancers such as gastric cancer. Other cutaneous manifestations of gastric cancer include tripe palms (a similar darkening hyperplasia of the skin of the palms) and the sign of Leser-Trelat, which is the rapid development of skin lesions known as seborrheic keratoses

Histopathology

Gastric adenocarcinoma is a malignant epithelial tumor, originating from glandular epithelium of the gastric mucosa. It invades the gastric wall, infiltrating the muscularis mucosae, the submucosa and thence the muscularis propria. Histologically, there are two major types of gastric cancer (Lauren classification): intestinal type and diffuse type.
Intestinal type adenocarcinoma: tumor cells describe irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma ("back to back" aspect). Often, it associates intestinal metaplasia in neighboring mucosa. Depending on glandular architecture, cellular pleomorphism and mucosecretion, adenocarcinoma may present 3 degrees of differentiation: well, moderate and poorly differentiate.
Diffuse type adenocarcinoma (mucinous, colloid): Tumor cells are discohesive and secrete mucus which is delivered in the interstitium producing large pools of mucus/colloid (optically "empty" spaces). It is poorly differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery - "signet-ring cell".

Staging

If cancer cells are found in the tissue sample, the next step is to stage, or find out the extent of the disease. Various tests determine whether the cancer has spread and, if so, what parts of the body are affected. Because stomach cancer can spread to the liver, the pancreas, and other organs near the stomach as well as to the lungs, the doctor may order a CT scan, a PET scan, an endoscopic ultrasound exam, or other tests to check these areas. Blood tests for tumor markers, such as carcinoembryonic antigen (CEA) and carbohydrate antigen (CA) may be ordered, as their levels correlate to extent of metastasis, especially to the liver, and the cure rate.

Staging may not be complete until after surgery. The surgeon removes nearby lymph nodes and possibly samples of tissue from other areas in the abdomen for examination by a pathologist.

TNM staging is used

Treatment

Like any cancer, treatment is adapted to fit each person's individual needs and depends on the size, location, and extent of the tumor, the stage of the disease, and general health. Cancer of the stomach is difficult to cure unless it is found in an early stage (before it has begun to spread). Unfortunately, because early stomach cancer causes few symptoms, the disease is usually advanced when the diagnosis is made. Treatment for stomach cancer may include surgery, chemotherapy, and/or radiation therapy. New treatment approaches such as biological therapy and improved ways of using current methods are being studied in clinical trials.

Surgery

Surgery is the most common treatment for stomach cancer. The surgeon removes part or all of the stomach, as well as some of the tissue around the stomach, with the basic goal of removing all cancer and a margin of normal tissue. Depending on the extent of invasion and the location of the tumor, surgery may also include removal of part of the intestine or pancreas . Tumors in the lower parts of the stomach may call for a Billroth I or Billroth II procedure. Endoscopic mucosal resection is a treatment for early gastric cancer that has been pioneered in Japan, but is available in the United States at some centers. In this procedure, the tumor is removed from the wall of the stomach using an endoscope, with the advantage in that it is a smaller operation than removing the stomach. Surgical interventions are currently curative in less than 40% of cases, and, in cases of metastasis, may only be palliative.

Chemotherapy

The use of chemotherapy to treat stomach cancer has no established standard of care. Unfortunately, stomach cancer has not been especially sensitive to these drugs until recently, and historically served to palliatively reduce the size of the tumor and increase survival time. Some drugs used in stomach cancer treatment include: 5-FU (fluorouracil), BCNU (carmustine), methyl-CCNU (Semustine), and doxorubicin (Adriamycin), as well as Mitomycin C, and more recently cisplatin and taxotere in various combinations. The relative benefits of these drugs, alone and in combination, are unclear.[10] Scientists are exploring the benefits of giving chemotherapy before surgery to shrink the tumor, or as adjuvant therapy after surgery to destroy remaining cancer cells. Combination treatment with chemotherapy and radiation therapy is also under study. Doctors are testing a treatment in which anticancer drugs are put directly into the abdomen (intraperitoneal hyperthermic chemoperfusion). Chemotherapy also is being studied as a treatment for cancer that has spread, and as a way to relieve symptoms of the disease. The side effects of chemotherapy depend mainly on the drugs the patient receives

Radiation therapy

Radiation therapy (also called radiotherapy) is the use of high-energy rays to damage cancer cells and stop them from growing. When used, it is generally in combination with surgery and chemotherapy, or used only with chemotherapy in cases where the individual is unable to undergo surgery. Radiation therapy may be used to relieve pain or blockage by shrinking the tumor for palliation of incurable disease

Multimodality therapy

While previous studies of multimodality therapy (combinations of surgery, chemotherapy and radiation therapy) gave mixed results, the Intergroup 0116 (SWOG 9008) study[11] showed a survival benefit to the combination of chemotherapy and radiation therapy in patients with nonmetastatic, completely resected gastric cancer. Patients were randomized after surgery to the standard group of observation alone, or the study arm of combination chemotherapy and radiation therapy. Those in the study arm receiving chemotherapy and radiation therapy survived on average 36 months, compared to 27 months with observation.

Duodenal cancer

2008-10-18T02:42:00.000-07:00

Duodenal cancer is a cancer in the beginning section of the small intestine. It is relatively rare compared to gastric cancer and colorectal cancer. Its histology is usually adenocarcinoma. Familial adenomatous polyposis (FAP) is a risk factor for developing this cancer.

The duodenum is the first part of the small intestine. It is located between the stomach and the jejunum. After foods combine with stomach acid, they descend into the duodenum where they mix with bile from the gall bladder and digestive juices from the pancreas.

Treatment

Resection is sometimes a part of a treatment plan,[1] but duodenal cancer is difficult to remove surgically because of the area that it resides in, there are many blood vessels supplying the lower body. Chemotherapy is sometimes used to try and shrink the canceous mass. Other times intestinal bypass surgery is tried to reroute the stomach to intestine connection around the blockage.

A 'Whipple' is a possible surgery that is tried sometimes with this cancer.

Some patients are fitted with tubes to either add nutrients (feeding tubes) or drainage tubes to remove excess processed food that can not pass the blockage.

Presentation

The cancerous mass tends to block food from getting to the small intestine. If food can not get to the intestines, it will cause pain, acid reflux, and weight loss because the food can not get to where it is supposed to be processed and absorbed by the body.

Patients with duodenal cancer may experience abdominal pain, weight loss, nausea, vomiting, and chronic GI bleeding.

Liver tumor

2008-10-18T02:36:00.001-07:00

Hepatic tumors are tumors or growths on or in the liver (medical terms pertaining to the liver often start in hepato- or hepatic from the Greek word for liver, hepar). These growths can be benign or malignant (cancerous). They may be discovered on medical imaging (even for a different reason than the cancer itself), or may be present in patients as an abdominal mass, hepatomegaly, abdominal pain, jaundice, or some other liver dysfunction.

Malignant (cancerous)

Most cases are metastases from other tumors, frequently of the GI tract (like colon cancer, carcinoid tumors mainly of the appendix, etc.), but also from breast cancer, ovarian cancer, lung cancer, renal cancer, prostate cancer, etc.
The most frequent, malignant, primary liver cancer is hepatocellular carcinoma (also named hepatoma, which is a misnomer because adenomas are usually benign).
More rare primary forms of liver cancer include cholangiocarcinoma, mixed tumors, tumors of mesenchymal tissue, sarcoma and hepatoblastoma, a rare malignant tumor in children.

Benign

-Hepatic Hemangioma are the most common liver tumors, found in up to 7% of autopsy specimens.
A rare tumor is Infantile hemangioendothelioma.
-Hepatic Adenoma, mainly in women using estrogens as contraceptives, or in cases of steroid abuse
-Focal Nodular Hyperplasia
Nodular regenerative hyperplasia
Hamartoma

Natural Self-Defense Against Breast Cancer

2008-10-13T09:03:00.000-07:00

Natural Self Defense Against Breast Cancer - Learning to Cope with Organochlorine Pollution

What are organochlorines?

Organochlorines are chemicals found in some herbicides and pesticides, in chlorine bleach and most chemical disinfectants, and many plastics, especially PVC (polyvinylchloride).

Organochlorines are implicated in causing and promoting breast cancer because they mutate genes and they cause breast cells to become more receptive to a cancer-promoting chemical called estradiol. Organochlorines weaken the immune system and lower your body’s resistance to bacteria and viruses. They also act as a negative type of estrogen in the body.

How do they enter our bodies?

Organochlorines enter our bodies through our drinking water, by eating foods grown with certain agricultural chemicals, and through the plastic linings on canned or microwaveable foods. They enter through our lungs by breathing in the fumes of chlorine bleach disinfectants and by body contact with chlorine bleached paper products such as tampons, toilet paper and paper cups.

How can we reduce our exposure?

Step One-Reduce Your Exposure

The first thing to do is to reduce your plastic consumption, especially of convenience foods. On plastic containers, there is typically a triangle with a number inside of it on the bottom of the container. You can recognize PVC or polyvinylchloride as the type of plastic that has a 3 in the center of the triangle.

As for paper products, use oxygen bleached or unbleached paper products. Companies who sell non-chlorine bleached paper products typically say so on the label and they do not necessarily market their products as “green” products.

Buy the non-chlorine bleach and more environmentally friendly household products. Simple vinegar and water can be used for many household chores.

Eating only organically produced meat and dairy products will reduce the amount of organochlorines in your diet by 80%.

Step Two-Help Your Liver

With help, your liver can metabolize organochlorines.

Flaxseeds and organic egg yolks contain lecithin, a chemical that speeds up the elimination of fat-soluble chemicals such as organochlorines by making them water-soluble.

Beans, lentils, red clover, soy products and chickweed contain chemicals called saponins. Saponins help to break down organochlorines, prevent cellular mutation and can stop the reproduction of cancer cells. These foods are strongly recommended for anybody who regularly consumes organochlorines.

Members of the cabbage family including broccoli, kale, turnips, radishes, cabbage, bok choy or cauliflower can help you metabolize organochlorines by increasing the production of non-cancerous by-products.

Step Three-Mother Nature’s Help

Woman-positive natural sources of estrogen can block entrance of organochlorines, estradiol and other cancer promoting estrogens when enough of them are in the blood stream. The reason behind this is that these positive hormones move quickly through our bodies whereas the cancer producing chemicals such as organochlorines move more slowly. If there are enough of these plant hormones in the blood stream, they can easily block organochlorines from attaching themselves to breast cells and from promoting cancer.

These plant hormones can be found in lentils, dried beans, tofu and fermented soy products such as tempeh and miso, parsnips, sweet potatoes, pomegranates, burdock roots, red clover, hops and ginseng. Regular intake of broccoli and cabbage is also helpful.

Post Transformation Tips

Making changes in favor of your survival and that of the environment often puts us in a period of re-adjustment, not only with the society we live in, but also with our family, friends and neighbors.

Several strategies we use to maintain positive social relations are

Natural self-defense does not mean natural aggression, nor does it mean that it will cause you to develop a social disorder triggered by the existence of organochlorines. Foods and herbs that encourage natural self-defense make you lose the taste for products associated with organochlorines.

Allow self-defense foods to empower you to envision and work towards an organochlorine free future without any anger about the present situation. In other words, don’t let the forces that encourage personal and environmental negligence push your buttons.

Chose recycled plastic toys or second hand plastic toys over new ones for your children.

Send lunches in reusable containers.

Bring a bean or lentil salad to the next barbecue or potluck supper.

Invite friends who use a lot of plastic and organochlorine products over to eat. Explain why you eat certain foods and what you have done to minimize your contribution to its proliferation. Relay the information in such a way that your guests feel comfortable and leave them to lose the taste for organochlorine products in their own way and time.

Use organic foods to show your body what a natural food is and have confidence that your body will use this knowledge to recognize what isn’t natural and respond appropriately to it. This is a goal that can be started even on a limited budget. The return of your natural body begins with one organic apple, especially a shared one!

Written by Jennifer Rodriguez-Allen, B.Sc., Environmental Chemist and President of Agoo Agii, inc (http://www.agooagii.com/). This article can found in print form with Agoo Agii's Aromatherapy Breast Self-Exam Kit. Gently encourage a loved one (or yourself) perform the Breast Self-Exam.

Legal Disclaimer-The information contained in this article is for educational purposes only and is not intended to medically diagnose, treat or cure any disease. Consult a health care practitioner before beginning any health care program.

Top Six Heart Healthy Foods

2008-09-12T11:11:00.000-07:00

Annual death tolls from sudden cardiac episodes among young women have risen nearly 30-percent since 1989, according to a recent study. Here are six foods that can lower your risk of heart disease.

1. Fish
(Can cut risk up to 50-percent)
The American Heart Association recommends eating at least two servings of fish a week. Research now shows that eating at least one serving of fish each week can cut your risk of dying from a heart-related disease in half.

2. Apples
(Can cut risk up to 50-percent)
An apple or two a day really may help keep doctor visits at bay. Research has shown that drinking 12 ounces of apple juice or eating two whole apples a day can reduce the oxidation of LDL cholesterol. Another study done in the Netherlands found that the phytochemicals in apples could help cut the risk of death from heart disease or stroke in half.

3. Walnuts
(Can cut risk up to 45-percent)
Walnuts contain a type of fat called linolenic acid, which lowers cholesterol and prevents blood clots. In fact, a study found that eating walnuts could decrease your total cholesterol level by 12 percent and LDL cholesterol level by 16 percent.

4. Olive Oil
(Can cut risk up to 40-percent)
Of all cooking oils, olive oil contains the largest proportion (77-percent) of monounsaturated fat, which lowers LDL cholesterol without affecting HDL levels. In cardiology-speak, that is called "improving your cholesterol ratio". Olive oil is obtained from the whole fruit, making it high in plant phenols, which are powerful antioxidants.

5. Legumes
(Can cut risk up to 30-percent)
One serving of dried beans a day can reduce cholesterol by up to 10-percent. The fiber is the primary protector. Beans also contain compounds that may reduce clotting and improve blood-vessel function. They are also a great source of folate, which keeps homocysteine levels (an indicator of heart trouble), in check. See also: Using the "Ol Bean.

6. Oats
(Can cut risk up to 29-percent)
According to more than 40 studies, eating about one-cup of cooked oatmeal a day significantly decreases blood cholesterol levels, thanks to beta-glucans, a soluble fiber. The key is to maintain a consistent intake; regular consumption of oatmeal cuts your overall heart-disease risk by as much as 20-percent.

Ten Ways to Good Nutrition

2008-09-12T11:05:00.000-07:00

1. The major dietary problem in the US and countries of the Western world is over-consumption of certain dietary components. Excessive intake of sugars and fats have resulted in excessive caloric intake together with a diet of low nutrient density. One in four Americans is obese, a risk factor for diseases of the heart, blood vessels, cancer, diabetes millitus and others.

2. The evidence that diets restricted in fat, saturated fat and cholesterol can reduce the incidence of chronic diseases is now overwhelming.
3. Learn to recognize the difference between hunger and appetite. Hunger is the stimulus within our bodies that indicates to us that we need to consume food. Appetite consists of the pleasurable sensations provided by food and is associated with the enjoyment of food.

4. Food is often used in one way or another to express feelings of happiness, love, security, or to cover up emotions of worry, grief, loneliness and so on. Before you have a snack, ask yourself why you need this snack, or why you may be reaching for something you know you should not eat.

5. There is a saying "A healthy body produces a healthy mind". This is true, because the brain benefits when food intake is adequate.

6. Support of family and significant other's is necessary for success.
7. Whatever you eat turns into YOU. Only you have complete control of what goes into your mouth.

8. Sugar. Be careful. It is very easy to eat excess amounts of sugary food raising your caloric intake too high. One 12 ounce can of a soft drink with sugar beyond your caloric requirement could cause a potential weight gain of almost 15 pounds in a year.

9. An important part of staying fit is controlling your body weight.

10. Food is anything that nourishes the body. No two foods are alike in the ability to nourish, for no two foods contain identical amounts of nutrients. Therefore, variety in your diet is important.

Easy Ways to Eat Your Vegetables

2008-09-12T10:53:00.000-07:00

-Keep frozen and canned vegetables on hand to know you always have vegetables at the ready.
-Make double and triple portions; at a serving one day and have one ready-to-go for the next.
-Keep a bag of pre-cut or baby carrots around -- grab a handful as a snack, pack them with lunch, throw them into stew, or microwave for a quick vegetable.
-Microwave or saute onions and peppers to put more vegetables into a tomato sauce
-Toss extra sauteed vegetables on a frozen pizza.
-Make a big salad to last a few days, store in the refrigerator in a plastic container.
-Add vegetables into sandwiches -- not just the old lettuce and tomato, try alfalfa sprouts, sliced red onion, sliced cucumbers, sliced yellow squash or zucchini, red peppers, or leftover grilled vegetables.
-Add vegetables to an omelette or scrambled eggs -- sauté onions, peppers, mushrooms, tomatoes and add some fresh herbs.
-Drink tomato, V-8 or Bloody Mary mix as a vegetable.
-In a tomato sauce, cut the amount of meat you use in half and add more vegetables -- onions, peppers, mushrooms, eggplant, zucchini or others

Tomato Sauce: Delicious Cancer Defense

2008-09-12T06:34:00.000-07:00

Tomato sauce, a common staple found in most pantries, has powerful health benefits thanks to an ingredient called lycopene. Lycopene is a phytochemical that acts as a powerful antioxidant, potentially helping to reduce the risk of prostate, esophageal and breast cancers. Lycopene is also a pigment. This pigment is what makes watermelon vivid pink and tomatoes bright red. You can also find lycopene in fresh papaya, guava, pink grapefruit and all other tomato products.

You will receive the best absorption of lycopene from cooked or processed products such as tomato-based pasta sauce, tomato paste, sauce, soup, juice, bottled salsa, chili sauce and ketchup. A bonus: When these foods are eaten with a little fat the lycopene is even better absorbed.

Rosy Couscous
When a box of couscous calls for 2-cups water or broth, use 1-1/4 cup water or broth and 1-cup pasta sauce instead. Serve the pasta as a side dish, or serve pork loin, fish steak or other entree on a bed of it.

Zesty Zucchini
Stew this vegetable in pasta sauce to boost flavor and nutrients. Try this: Slice one large zucchini into 1/4-inch thick slices. In a covered saucepan over medium heat, simmer the slices in 1/2-cup of your favorite pasta sauce for five minutes or until the zucchini is cooked through.

SaucySoup
In a large saucepan, add One can of (15 to 16-ounce) low-sodium chicken broth, one can of (15 ounce) drained white beans, 1-cup pasta sauce (with garlic) and 1-cup chopped leftover cooked chicken or turkey breast. For a taste variation, add a few pinches of dried, crushed rosemary. Bring the soup to a boil over medium-high heat. Season with salt and pepper and serve.

A favorite fact: Pizza is loaded with lycopene!

Prepare sauce or use sauce from a can or jar if pressed for time.

Italian Dip
Savor your dip with a large, leafy green salad topped with white beans, cherry tomato halves and a splash of balsamic or red wine vinegar. Go for a sweet ending with watermelon, if desired.

Ingredients:
1 pound extra lean ground round
1-1/4 cup jarred tomato-based pasta sauce
1/2 teaspoon ground black pepper
1/4 teaspoon garlic salt
1/2 pound loaf fresh Italian bread, cut into eight 1-ounce slices
1/2 cup shredded part-skim mozzarella cheese
1/2 cup fresh basil leaves (12 to 16 large leaves)

Combine the beef, 1/2-cup sauce, pepper and garlic salt in a mixing bowl. Divide and shape the mixture into four patties.

Place a large nonstick skillet over medium-high heat. When hot, cook the burgers for four to five minutes per side for medium, six minutes per side for well done.

While the burgers are cooking, heat the remaining 3/4-cup sauce in a saucepan over medium heat.

When the burgers are cooked to the desired doneness, place each onto a bread slice. Immediately top with the cheese and basil, then cover with the remaining bread slices. Serve each burger with the warm sauce as a dipping sauce.

Recipe makes four sandwiches.

Nutrition Information per serving:
Calories: 436
Protein: 36g
Carbohydrate: 36g
Fat: 14g
Cholesterol: 84mg
Fiber: 3g
Sodium: 830mg

Eight way to prevent cancer

2008-08-26T04:46:00.000-07:00

1. Don't smoke
In the United States, smoking causes approximately 30 percent of all cancers and 90 percent of lung cancers. About half of all smokers will die from a smoking-related disease, like cancer, heart disease, and chronic obstructive lung disease. Globally, tobacco is estimated to cause just under five million deaths a year – a number that will likely rise dramatically over the next two generations 6, 7.
Linked primarily in the public’s mind with lung cancer, smoking and use of smokeless tobacco greatly increases the risk of many other cancers, including cancer of the head and neck, bladder, kidney, cervix, esophagus, pancreas, stomach, colon, rectum, and blood (certain leukemias)8.

The single best way to prevent cancer and other chronic diseases is not to smoke. In the United States alone, over 150,000 cancer deaths could be avoided each year if tobacco were somehow miraculously eliminated from the earth9.

Preventing teens and young adults from taking up smoking provides the biggest health benefits, yet despite stepped up efforts to prevent tobacco use, over 20 percent of the United States population still smokes10. Because of this, efforts to get smokers to stop smoking (cessation) have become increasingly common as well, yet only a small percentage of those trying to quit seek effective treatments that can help them stop11. Despite this, cessation has huge benefits. Within two years of quitting, the risk of many smoking-related diseases begins to drop, and after 10 – 20 years, the risk of lung cancer and most other tobacco-related diseases nearly equals that of non-smokers.

2. Maintain a healthy weight

Although weight is one of the most important risk factors for cancer, a recent survey commissioned by the American Cancer Society found that less than 10 percent of the public were aware that being overweight could increase the risk of cancer12. Very good evidence shows, though, that about 90,000 deaths from cancer could be avoided each year in the United States if everyone stayed at a healthy weight throughout life13.

Carrying extra weight, particularly being obese ( defined as BMI greater than or equal to 30) (BMI calculator), has been strongly linked to an increased risk of cancers of the breast (after menopause), colon, kidney, pancreas, and esophagus (adenocarcinoma). And there is growing evidence that obesity also increases the risk of leukemia, lymphoma, multiple myeloma, and cancers of the liver and gallbladder
The way weight increases cancer risk varies from cancer to cancer. For example, estrogen produced by fat cells likely increases risk of postmenopausal breast cancer; blood sugar and insulin problems linked to being overweight likely increases risk of colon and pancreatic cancer; and weight-related irritations caused by gallstones and acid reflux likely increase the risk of cancers of the gallbladder and esophagus, respectively.

The now well-known and disturbing trends in the prevalence of overweight and obesity in the United States predict a growing burden of not only weight-related cancers but also heart disease, stroke, and diabetes. The latest data show that a full two thirds (66 percent) of the population is either overweight (BMI 25 – 29.9) or obese (BMI greater than or equal to 30)14. Over the last two decades, rates of obesity have significantly increased across the nation, with about a third of the population now considered obese (figure 2)14, 15. Such trends, while most pronounced in the United States, are being expressed worldwide as well, pointing to a huge future global burden from weight-related diseases.

Unfortunately, these trends show no sign of letting up and point to the need for a paradigm shift in weight control efforts, one modeled much more on national tobacco control efforts than individual action. Such efforts are slowly beginning to surface16, 17, but much more widespread, cohesive policy initiatives will be needed to stem the tide of weight gain and then begin to reverse it.

3. Exercise regularly

The health benefits of regular physical activity are well known. In addition to lowering the risk of heart disease, stroke, diabetes, osteoporosis, and high blood pressure, it also helps prevent cancer. Overall, in the United States, it’s estimated that five percent of cancers are linked to lack of regular exercise, which is largely accounted for through the link with two common cancers, breast cancer and colon cancer 3.

For breast cancer, the benefits of regular exercise seem biggest for premenopausal women, but postmenopausal women see lower risks from regular physical activity as well. It’s believed that the lower lifetime exposure to estrogen caused by regular exercise is the main reason exercise helps prevent the disease. High lifetime exposure to estrogen is a known risk factor for breast cancer. Though data are still developing, some researchers theorize that childhood activity level may be even more important than adult activity, as this is a key time in growth and development. Active girls tend to begin menstrual periods (menarche) later in life and tend to be leaner than other girls, two factors that can lower lifetime exposure to estrogen.

For colon cancer, the main mechanism seems to be that exercise can help control insulin levels, which can keep in check certain hormones and growth factors that can promote cancer in colon tissue.

For all its benefits, activity is not the preferred pastime of most people in the United States. Over 50 percent of the population doesn’t get the recommended amount of activity each week – either 30 minutes of moderate activity (like brisk walking) five or more days per week, or 20 minutes of vigorous activity (like running) three or more days per week18. Approximately 15 percent of the population is almost completely inactive18.

4. Eat a Healthy Diet
A healthy diet is key to overall health and can help lower the risk of many cancers. While news coverage of the links between diet and cancer have been confusing at best, and misleading at worst, there is solid evidence that the way we eat has a real impact on cancer risk. Perhaps surprisingly, it’s not fat or meat, or fruits and vegetables that is the most important part of diet when it comes to cancer risk; it’s simply calories19. Keeping calories in check, so weight stays in check, is the single most important change in diet people can make. Outside of calories, good evidence shows that a risk reducing diet is: largely plant based (with a lot of fruits, vegetables, and whole grains); low in animal products (like animal fat, red meat, and processed meat); low in sodium; and, for men, not too high in calcium (less than 1500mg/day)20 .

A daily multivitamin with folate can provide added protection against certain cancers and other chronic diseases21, 22. Folate is a B vitamin that has been shown to lower the risk of colon cancer, as well as breast cancer in women who regularly drink alcohol. The calcium and vitamin D in most multivitamins may also help provide added protection against colon cancer.

Cancers with a link to diet include: breast cancer, colon cancer, esophageal cancer, lung cancer, oral cancer, pancreatic cancer, prostate cancer, and stomach cancer, as well as kidney and uterine cancer, which are linked through weight gain 4, 20, 23.

5. Drink alcohol in moderation, if at all

Alcohol plays a perplexing role in health. While studies consistently show that drinking even a small amount of alcohol (less than one drink/day) can raise the risk of two common cancers (breast and colon), there’s also very good evidence that moderate consumption can significantly lower the risk of cardiovascular disease24.

Balancing these risks and benefits is key to pubic health messages about alcohol intake:

Although the benefits of moderate intake are well established, the cancer risk and potential for alcohol dependence means that non-drinkers should not be encouraged to start drinking.

Most of those who already drink moderately, though, don’t need to be encouraged to stop. While cancer risk may be increased slightly in this group, the cardiovascular benefits are significant as well.

All heavy drinkers should be encouraged to cut back to moderate levels, or stop altogether.
For both breast cancer and colon cancer, alcohol likely increases risk by lowering levels of folate in the body, though there are other possible reasons. Folate has been shown in some studies to protect against cancer. The lower levels caused by alcohol may therefore increase risk. Good evidence, though, shows that taking a folate supplement (like a multivitamin) can help eliminate some of the cancer risk linked to alcohol25-27.

6. Protect yourself from the sun

Too much sun exposure is a well-known cause of skin cancer, including serious melanoma. With melanoma rates rising steadily from year to year both in the United States and worldwide, proper sun protection is a key public health message. Yet in the United States, an increasing number of people are experiencing severe sun exposure. The percent of the population reporting a sun burn over the past year is rising, with a third reporting at least one sunburn, and about 20 percent reporting four or more 28.

Clearly, such severe exposure is unsafe and greatly increases the risk of cancer. Less clear, however, are the health hazards from very mild sun exposure. Growing evidence shows there could be some overall benefits from five to 30 minutes of unprotected sun exposure twice a week29. While there is likely some skin cancer risk from such light exposure, there may be a number of health benefits as well. Sunlight causes the formation of vitamin D in the skin, and there is some good evidence that vitamin D can help protect against osteoporosis and colon cancer, and possibly cancers of the prostate, breast, and ovary as well29-31.

Taken together, the evidence on vitamin D’s benefits seems to point to a need to rethink current sun exposure recommendations, which are likely too restrictive to provide much, if any, of the cancer prevention benefits of vitamin D. However, until there’s a clear paradigm shift, caution is in order, and the public should be encouraged to properly protect themselves (and their children) from the sun whenever possible, which includes: avoiding the sun as much as possible during peak burning hours (10am – 4pm); wearing long sleeve shirts, long pants, and wide-brimmed hats, and; properly applying broad-spectrum sun screen.

7.Protect yourself from infections
Although not well known by the general public, infections play an important role in the development of some cancers. Worldwide, approximately 15 percent of all cancers have been linked to infections. In developing countries, this number reaches almost 25 percent32.

Certain infections can either directly or indirectly cause changes that can lead to cancer. This can happen because of the chronic inflammation that some infections cause or by an infectious agent (like a virus) changing the behavior of infected cells. Infections that compromise the immune system (like HIV) also increase cancer risk by making the body less able to defend against infections that can cause cancer.

Not surprisingly, infection-associated cancers are not a health burden borne equally by all. The poor living conditions and inadequate health care experienced by many people worldwide increase the likelihood of cancer resulting from chronic infections.

There are at least ten infectious agents that are known to increase the risk of cancer (see table), and several of them are quite common. Yet, in most instances, only a small proportion of those infected actually go on to develop cancer because it takes a unique set of factors along with the infection to turn normal cells cancerous.

Still, these infectious agents have a substantial impact on cancer worldwide. Of particular importance are human papillomavirus (HPV), hepatitis B and C viruses, and Helicobacter pylori. HPV is a sexually transmitted virus that is linked to numerous cancers, with cervical cancer being the most important. It’s estimated that almost all cervical cancers are caused by HPV infection. Hepatitis B and C infect the liver and together account for the large majority of liver cancer. Finally, Helicobacter pylori, a bacteria that infects the stomach, has been estimated to cause upwards of 75 percent of all stomach cancers, the second most common cancer worldwide.

The promise of prevention is a bright spot when looking at the reach of infection-associated cancers. To lower their risk, individuals can take concrete steps like avoiding blood exposure (by not sharing needles, for example), practicing safer sex and, for women, getting regular Pap tests (which test for cervical cancer). There is also very strong evidence that vaccinating girls (around age 11 or 12) against HPV can greatly reduce the risk of cervical cancer later in life 33. Growing use of the hepatitis B vaccine worldwide is expected to result in similar benefits in liver cancer34. Advances on vaccines for other agents also offer much hope for prevention.

8.Get screening tests regularly

Having cancer screening tests at regular intervals is the single best way to protect against cancer. Not only can screening tests find cancers early when they’re most treatable, in the case of colon and cervical cancer they can actually help prevent the disease.

Screening tests for colon cancer help prevent cancer by finding and removing adenomatous polyps, which are abnormal growths that can go on to become cancer. Regular screening with sigmoidoscopy, for example, has been shown to cut the risk of dying from colon cancer in half; fecal occult blood tests can cut colon cancer mortality by up to a quarter35. Although an increasing proportion of adults 50 and older in the United States is actually getting screened for colon cancer, close to 40 percent are still missing recommended tests36.

Rates of screening are much better for the Pap test, which screens for cervical cancer. Over 80 percent of the age-eligible women in the United States have had a Pap test within the last three years, which generally meets current guidelines. Pap tests help find abnormal changes in the cells lining the cervix, which could go on to be cancerous. The abnormal cells can then be treated or removed. The Pap test is a huge success story of public health. From the time it became widely used in the 1950’s, rates of death from cervical cancer have dropped by over 70 percent in the United States and other developed nations.

A recent addition to cervical cancer screening is the human papillomavirus (HPV) test, which can be offered to women beginning at age 30 in addition to their regular Pap test. The tests detects whether a woman has an infection with a high-risk type of HPV that is strongly linked to cancer. Women with these high-risk types can then have additional follow-up tests to look for abnormal changes to cells in the cervix.

Outside of prevention, screening tests are key to finding cancer early when it is most treatable, Breast, cervical, and colon screening should be priorities for women. Colon and possibly prostate screening should be priorities for men. The American Cancer Society recommends a number of tests that protect against cancer. In addition to the specific tests generally laid out below (see tables37), doctors should also perform an occasional exam for signs of cancer of the thyroid, testicles, ovaries, lymph nodes, oral cavity, and skin. Those at increased risk for a specific cancer may need to begin screening earlier, and get screening tests more often, than is recommended for most people.

Cancer Prevention

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Over half of all cancers can be prevented by a combination of healthy lifestyles and regular screening. This is a key message for a disease that is overwhelmingly the public’s number one health fear. Eight simple behaviors can greatly lower cancer risk as well as help prevent other serious diseases, like heart disease, stroke, diabetes, and osteoporosis.

Eight Ways to Prevent Cancer

Most cancers can be prevented. This is a key message for a disease that is overwhelmingly the public’s number one health fear1. Unfortunately, it’s also a message that nearly half of the public doesn’t take to heart or even really believe1.
Yet, beginning with Doll and Peto’s groundbreaking analyses in the 1980’s, overwhelming evidence now shows that over half of all cancers – and up to three quarters of some specific cancers - could be avoided by a combination of healthy lifestyle and regular screening .
Although this conclusion is now agreed upon in nearly all scientific circles, it took some visionary thinking and research to bring us to this point. The first studies that convincingly initiated the idea that cancer risk was something partly under a person’s control came from studies that compared the rates of cancer in different countries around the world. These so called ecologic studies found that rates of cancer can vary wildly from population to population. And while these differences could have been due in part to genetics and environmental exposures, they also pointed to the potential importance of lifestyle in cancer risk – a hypothesis made even more compelling by another set of groundbreaking studies looking at the cancer risk of migrants as they moved from low risk countries to high risk countries. These studies have found that migrant groups slowly take on the cancer risk profiles of the countries they move to, and the longer they stay there, the more their risk resembles that of the typical population (figure 15). That the genetic make-up of these groups doesn’t change over time, the change in cancer risk points largely to the importance of lifestyle.

Adding even more weight to the argument are the numerous studies clearly showing that certain lifestyle changes can lower cancer risk, such as research into the benefits of quitting smoking. Finally, randomized controlled trials show that drugs like Tamoxifen can cut breast cancer risk in half and that vaccines can prevent both cervical and liver cancer.

Taken together, the current evidence on cancer prevention points to eight simple behaviors that can greatly reduce overall cancer risk. While there are additional steps that can reduce the risk of some individual cancers (see Fourteen Preventable Cancers), these eight behaviors provide the greatest benefit for the most cancers and can also go a long way toward reducing the risk of other serious chronic diseases, like heart disease, stroke, diabetes, and osteoporosis.

Genetic Testing in Cancer Patients

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There are two major reasons to test a cancer patient for gene mutations causing a hereditary cancer syndrome. First, finding such a genetic alteration affects patient care. Individuals known to have a hereditary cancer syndrome are at much higher risk for additional tumors later in life and, therefore, prophylactic surgery or heightened surveillance is often necessary to prevent additional cancers or to find these cancers early when they are more treatable. Secondly, knowing the specific mutation allows the identification of those relatives who either are or are not at the same increased risk for cancer as their affected relatives, so they can receive appropriate counseling and care.

Not all patients with cancer need genetic testing, however. Whether to do genetic testing depends on a number of factors including (1) the type of cancer, (2) other features of the cancer such as the age of onset and whether it was bilateral or arose at more than one primary site, (3) other physical features besides the cancer itself that are known to be associated with a hereditary cancer syndrome, and (4) the patient’s family history and ethnicity. At one end of the spectrum is a patient whose cancer is of a kind that is recognized as frequently the result of inherited mutations in a known gene, especially when the patient’s relatives have cancers that are known to be related to the kind of cancer the patient has. For example, in retinoblastoma, there is only one gene, RB1, in which mutations cause the disease. A patient with bilateral retinoblastoma whose parent, uncles or siblings have also had the disease, is very likely to have inherited a mutation in the RB1 gene and to be carrying the mutation in all the cells of his body. Genetic testing to find the specific mutation in RB1 is often done in this situation.

At the other end of the spectrum is a patient with little or no family history of cancer whose own cancer is of a type that is rarely part of a hereditary cancer syndrome and for which no gene mutation is known. For example, no genetic testing is currently recommended for a patient with lung cancer and no family history.
Between these two ends of the spectrum are cancers of the breast, kidney, and colon, among others, in which less than 5% of all such cancers occur as part of a hereditary cancer syndrome. In these situations, the genetic counselor collects a lot of information about the cancer and the family history to assess whether the cancer in this particular patient is more or less likely to be part of a hereditary cancer syndrome for which testing is available. In some cases, there are a variety of software tools that aid in this assessment. In general, if the characteristics of the cancer and the family history together raise the chance there is a hereditary cancer syndrome from less than 5% to 10% or greater, genetic testing of the appropriate gene or genes is performed. Once again, knowing there is a mutation in a particular gene associated with a hereditary cancer syndrome can be extremely important for managing the patient’s disease, designing further surveillance measures, and testing relatives for their risk. In contrast, an individual who tests negative for a gene mutation responsible for cancer in a relative could forgo any special medical interventions or surveillance. However, it is important to stress that this does not mean the individual is at no risk for his relative’s cancer. It only means his or her risk drops down closer to the population risk. So, for example, a woman with a BRCA1 mutation has a 60-80% lifetime risk of developing breast cancer. A sister who tests negative for this BRCA1 mutation still has an approximately 10-15% lifetime risk of breast cancer, slightly above the risk of any woman in the general population.

What Kinds of Mutated Genes Cause Cancer?

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Three broad categories of genes are implicated in cancer: oncogenes, tumor-suppressor genes (TSGs) and cell-death genes. An oncogene is a cancer-causing gene that is an altered (“mutant”) version of a normal gene known as a cellular proto-oncogene. Proto-oncogenes are required for normal development and function. They provide the information, the genetic blueprints, for a large number of different proteins involved in promoting normal cell division. Cell division is a normal process that allows a single fertilized egg to divide and develop into the estimated 100 trillion cells that make up the specialized tissues and organs in an adult. Tissues must also have some cells that are able to divide to repair damage and replace cells that are lost during normal wear and tear. Proto-oncogenes are normally carefully regulated during development, tissue repair, and cell replacement so just the proper number of cell divisions occurs to generate the right number of new cells within a tissue and organ. An oncogene is an “activated” proto-oncogene in which a mutation has destroyed its ability to be regulated, and, as a consequence, it drives excessive cell division and the accumulation of cells that can form a tumor. Mutations in over 50 known proto-oncogenes are capable of causing cancer. Mutation of only one of the two copies of any proto-oncogene that changes it into an oncogene in a cell is sufficient to set that cell on the path to becoming malignant regardless of the presence of the other, normal non-mutated copy of the proto-oncogene.

Activating mutations in proto-oncogenes can explain why certain tumors can occur in both hereditary and sporadic forms. For example, some families have a rare form of cancer of the wall of the stomach, called gastric stromal tumor (GIST), as part of a hereditary cancer syndrome in which a risk for the cancer is inherited from parent to child. In these families, if a parent carrying an activating mutation in a proto-oncogene called KIT passes the mutant gene to a child, that child carries the abnormal form of KIT in all the cells of his body and is at high risk of developing GIST. Because the mutant KIT was present at the beginning in the fertilized egg, having been contributed either by the egg or sperm, DNA obtained from any tissue from anyone who inherited a mutant KIT gene would reveal one normal and one mutant KIT gene. In other individuals with GIST, however, the tumor is sporadic and not familial. These individuals start life as a fertilized egg with two normal copies of the KIT gene, one from each parent, but, later in life, one copy of the KIT gene in a cell in the stomach wall underwent an activating somatic mutation and became cancerous. Because the activating mutation in KIT occurred only in a cell within the stomach wall of an individual with the non-familial form of GIST and not in any other tissues of the body, testing the DNA obtained from the GIST tumor itself would reveal one normal and one mutant KIT gene while DNA from any tissue other than the tumor itself would reveal two normal copies of the KIT gene.

Tumor Suppressor Genes (TSGs)

A second category of gene implicated in cancer is the tumor suppressor gene (TSG). TSGs provide the genetic information for a large number of different proteins involved primarily in preventing cancer. Some are referred to as "gatekeepers" because they normally regulate and control cell division and, therefore, block the growth of the cancer. Loss of function of both copies of a TSG in a cell leads to uncontrolled cell division. Loss of function of a TSG usually comes about through a genetic change ("mutation") in the gene sequence itself. However, another mechanism for loss of function of a TSG is gene silencing that results from modification of the DNA or the proteins in which the DNA is packaged, thereby rendering the gene inaccessible to the cellular machinery that reads gene sequences. This type of gene silencing is referred to as "epigenetic" silencing because no mutation in the sequence of the gene occurs. Other TSGs, referred to as "caretakers", are involved in maintaining normal structure and number of chromosomes, repairing DNA damage, and preventing mutations. Loss of function of both copies of a caretaker TSG leads to cancer indirectly by allowing additional secondary mutations to accumulate that either activate proto-oncogenes or inactivate gatekeeper TSGs. These secondary mutations fuel the vicious cycle of genetic change in cancer since malignancy increases genetic damage and instability, which in turn leads to increased malignancy. As with the gatekeeper TSGs, both copies of a caretaker TSG must be inactivated in order for a cell to completely lose the caretaker function of that gene.

Inherited Gatekeeper Gene Mutations in Hereditary cancer syndromes: Retinoblastoma and the Two-Hit Model for Cancer

If a cell must lose both functioning copies of a TSG to lose the gatekeeper or caretaker function of the protein encoded by that TSG, how is it then that individuals affected with most hereditary cancer syndromes need only inherit one defective copy of a TSG to develop the cancer? Why doesn’t the other, normal copy make enough of the protein to prevent complete loss of the gatekeeper or caretaker functions? The explanation is best demonstrated with the example of retinoblastoma, a cancer of the retinoblast, the cells in the embryo that develop into the retina at the back of the eye. Retinoblastoma occurs in 1 in 20,000 infants and small children and is part of a hereditary cancer syndrome 40% of the time, and occurs as a sporadic cancer 60% of the time. In familial retinoblastoma, a person starts life as a fertilized egg with one inherited, defective copy of the RB1 gene, a well-known gatekeeper TSG. As a result, every cell in his body that develops from that fertilized egg also has one defective copy of the RB1 gene (Figure 2). In a small number of retinoblasts, a second “hit” occurs during cell division and development that inactivates the other, normal copy of RB1. As a consequence of this second hit, the cell loses the function of both copies of RB1, giving rise to a tumor. The second hit is most often a mutation, although loss of function without mutation, such as occurs when a gene is shut off inappropriately can also occur. Although a second hit is a rare event, all it takes is one second hit in any of the approximately one million retina cells already carrying one dysfunctional RB1 gene for a tumor to develop from that cell. In fact, because these second hits are rare, but not vanishingly so, they can occur in more than one retinoblast. As a result, patients with familial retinoblastoma are frequently young infants who develop more than one independent primary retinoblastoma tumor, either within one eye or in both eyes. Furthermore, because every cell of the body already carries one defective RB1 gene, a second hit later in life also results in a cell lacking function of the RB1 gatekeeper. In fact, children who survive retinoblastoma as part of a hereditary cancer syndrome have an 80-90% risk of developing cancers of bone, muscle, and connective tissues over their adult lifetimes.
In the sporadic, non-familial form of retinoblastoma, both copies of RB1 in a cell are also inactivated, but the inactivation results from two independent events occurring in the same cell. The loss of both copies of RB1 independently of one another in the same cell is a very rare event, equivalent to “lightening striking twice” in the same cell. As a result, the sporadic form of retinoblastoma occurs at only one location, in one eye, and generally when children are toddlers. As one might also predict, because survivors of the non-familial form of retinoblastoma are not carrying a defective RB1 gene in their other cells, they are not at greatly increased risk for cancers of bone, muscle, and connective tissues later in adulthood.

Inherited Caretaker Gene Mutations in Hereditary Cancer Syndromes: the Example of Familial Breast Cancer

Breast cancer is common. Up to 10% of all women in North America and Western Europe will develop breast cancer in their lifetime. In approximately 3% of cases, the cancer is due to an inherited mutation in one of two caretaker TSGs, known as BRCA1 and BRCA2. Women carrying a disease-causing mutation in BRCA1 or BRCA2 have a 60-90% risk lifetime risk of developing breast cancer and a 30-50% risk of ovarian cancer. In males, mutations in BRCA1 and BRCA2 account for 10-20% of all male breast cancer, which affects nearly 0.1% of males in the population, and increase the risk of prostate cancer. BRCA1 and BRCA2 families demonstrate features characteristic of other hereditary cancer syndromes: there are multiple affected individuals in a family with more than one type of cancer, the age at onset is earlier compared with the average in the population at large, and cancer in both breasts is frequent.

Inherited Caretaker Gene Mutations in Hereditary Cancer Syndromes: Familial Colon Cancer

Approximately 2-4% of cases of colon cancer are attributable to a group of hereditary cancer syndromes known as hereditary nonpolyposis colon cancer (HNPCC). HNPCC is characterized by inheritance of colon cancer occurring during adulthood, but at a relatively young age. Males carrying a mutant HNPCC gene have an approximately 90% lifetime risk of developing cancer of the colon; females have a somewhat smaller risk, approximately 70%, but have an approximately 40% risk for endometrial cancer. There are also additional risks of 10-20% for cancer of the bile ducts, the urinary tract, and the ovary.

HNPCC is a group of five similar hereditary cancer syndromes caused by mutations in one of five distinct genes that contain the blueprints for five DNA enzymes responsible for repairing certain kinds of DNA damage. As such, the HNPCC genes are prototypical caretaker TSGs. Although all five of these genes have been implicated in HNPCC in different families, two of these genes, MLH1 and MSH2, are together responsible for the most cases of HNPCC.

Tumor Suppressor Genes in Sporadic Cancers

The “two-hit” model of loss of function of a TSG is now widely accepted as the explanation for hereditary cancer syndromes besides retinoblastoma, including in familial breast cancer and HNPCC. The importance of TSGs and the two-hit model for explaining many features of the hereditary cancer syndromes goes way beyond these relatively rare syndromes. As with the example of retinoblastoma, the two-hit model also explains how loss of function of a TSG occurs in the more common sporadic forms of cancer. For example, there is a rare hereditary cancer syndrome known as Li-Fraumeni syndrome in which multiple family members in early- to mid-adulthood develop one or more cancers of bone or muscle, breast, and adrenal gland, as well as brain tumors and leukemia. Li-Fraumeni syndrome is usually caused by the inheritance of mutations in an important TSG known as TP53, a critical regulator of a cell’s response to DNA damage. Although the Li-Fraumeni syndrome is rare, mutations causing a loss of function of both copies of TP53 turn out to be one of the most common genetic alterations in all sporadic cancers. Mutations or deletion of both copies of the TP53 gene are frequent in a wide range of sporadic cancers, including breast, ovarian, bladder, cervical, esophageal, colon and rectal, skin, liver, and lung cancers, glioblastoma of the brain, and cancer of the bone.

Other TSGs have also been implicated in sporadic cancer. There is mutation or loss of expression of both copies of one or more of these DNA repair genes in up to 12% of sporadic colon cancer. BRCA1 and BRCA2 in sporadic breast cancer present a somewhat more complex situation. A mutation of one copy of BRCA1 or BRCA2 occurs in approximately half of sporadic breast cancer but the other copy of BRCA1 or BRCA2 is generally not lost or mutated. What has been found, however, particularly in more malignant forms of breast cancer, is a marked reduction in the amount of protein product made from what appears to be unaltered copies of BRCA1 or BRCA2. This reduction may be associated with changes in the way the genetic information is extracted from the genetic blueprint contained in the gene rather than with the gene itself.

Cell-Death Genes

During the normal processes of development, certain cells are supposed to be eliminated by a natural program of cell death, most commonly known as apoptosis. If cells fail to undergo programmed cell death normally, they will accumulate and ultimately result in cancer. The best-known example of a failure of programmed cell death in cancer is in a sporadic form of cancer of the white blood cells known as B-cell leukemia. Certain B-cell leukemias carry a major alteration in the genetic material such that a gene that suppresses cell death, called BCL2, continues to function when it was supposed to be shut off. As a result, white blood cells that were supposed to die and be eliminated remain alive and accumulate, ultimately leading to cancer.

Cancer Genetics

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What is Cancer?
Cancer is not a single disease, but rather, is the name used to describe the most dangerous form of neoplasia, a disease process characterized by abnormal, uncontrolled cell division leading to a mass or tumor. Uncontrolled growth alone, however, does not make a tumor a cancer. For a tumor to be a cancer, it must not only grow inappropriately at the site where it originates (the primary) but must also demonstrate malignant behavior, that is, the capacity to invade normal tissues neighboring the site of the primary tumor and/or to seed new tumors at distant sites in the body (metastases). The surrounding normal tissue is also likely to play an important role, by providing the blood supply that nourishes the tumor, by permitting cancer cells to escape from the tumor and form metastases, and by shielding the tumor from attack by the body’s own defense mechanisms. Thus, cancer is a complex process, both within the tumor and between the tumor and the normal tissues that surround it.

Cancer is a Disease of the Genes

Cancer is fundamentally a genetic disease, that is, the disease starts and progresses because of changes in the DNA sequence of certain genes, resulting in abnormal genetic information inside the cancer cells that is then passed on to the progeny of these abnormal cells as the cancer cell divides. Most of the time, these abnormalities in the genetic material are the result of what are referred to as somatic mutations (from the Greek word “soma” meaning body and the Latin word “mutare” meaning change). Somatic genetic changes occur in all cancers. In contrast to somatic mutations, mutations that are inherited through the fertilized egg are passed on to every cell of the body and are referred to as germline mutations.

Most cancer is sporadic, that is, it occurs once in a single individual and not multiple times in the patient and his relatives. In a few percent of cancers, more than one person in a family may develop the same or a related form of cancer. Of course, families in which two or more individuals develop one or more related types of cancers may simply represent a coincidence of two independent sporadic cancers, but there is also the possibility that they have a familial or hereditary form of the disease. In such families, individuals can inherit genetic abnormalities as germline mutations that strongly predispose to cancer and they carry these changes in every cell of their bodies. Regardless of whether a cancer is sporadic or hereditary, or whether the genetic changes are somatic or germline mutations, cancer results from alterations in the genetic material in the cancer cells that cause the cells to become and remain cancerous.

Although mutation in a single gene can initiate a cancer, many more genetic changes must occur to produce a fully malignant cancerous tumor. Rapid and unregulated cell division in the tumor cells leads to additional genetic abnormalities such as an abnormal number or structure of chromosomes, which creates imbalances in the genetic content of the cell, or additional mutations, which damage the structure of important genes. Although some damage kills cells or has no effect on cell survival, genetic changes that increase the growth rate of the tumor and confer the ability to invade surrounding tissue and send metastases to distant sites will cause cells to outgrow other cells in the neoplasia. The cells that experience an enhancement of growth and survival will come to predominate as the cancer evolves and progresses. Genetic damage that occurs in cancer cells sets up a vicious cycle because it reduces the cells’ ability to repair future genetic damage. Thus, the more malignant the cells become, the more their DNA is subject to damage, the more genetic damage accumulates, and the more malignant the cells become. It is in this sense that cancer evolves as a “genetic” disease because alterations in the integrity and functioning of genes are central to its initiation and progression.

Cancer in Families
Many forms of cancer have a higher incidence in relatives of patients than in the general population. For example, a woman’s risk of developing breast cancer is increased up to three-fold if one first-degree relative is affected. A family history of cancer in an individual’s parents, brothers or sisters should arouse suspicion of increased cancer risk in that person. Most of the time, the increased risk of cancer in family members results from the combined effect of changes in many genes, most of which are unknown or poorly understood, that increase cancer susceptibility. There are, however, some families with many relatives with cancer because they have what is referred to as a hereditary cancer syndrome (Figure 1). In a hereditary cancer syndrome, all it takes is for a person to be carrying an alteration in just one of a few dozen currently known hereditary cancer syndrome genes to have a markedly increased risk of cancer. In a hereditary cancer syndrome, the great majority of individuals carrying the gene alteration responsible for the disease will develop cancer. In addition to having multiple relatives affected with the same or related form of cancer, patients with a hereditary cancer syndrome typically develop their disease at an earlier age than what is seen in the general population and can have more than one independent primary tumor occurring at multiple sites or at different times. For example, patients with hereditary breast and ovarian cancer syndrome may have a breast cancer and an ovarian cancer occurring years apart, or breast cancer occurring simultaneously in both breasts.

Because the risk of developing cancer is so high in a person carrying a gene alteration responsible for a hereditary cancer syndrome, any relatives of a person with a hereditary cancer syndrome who share this altered gene have a similarly high risk of cancer. Identifying the gene alteration responsible for disease in a hereditary cancer syndrome family allows physicians to identify at-risk family members and provide more intensive screening, more effective prevention, and more successful treatment earlier in the course of the disease.

Radiation

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For women undergoing breast conserving therapy in the U.S., breast conserving radiation therapy has been classically given to the entire breast over approximately 6 weeks, followed by a “boost” to the specific site of the primary for approximately 2 more weeks, for a total of 8 weeks of radiation therapy. However, recent studies have suggested that perhaps only the site of the primary cancer needs to be treated, which is called partial breast radiation. Partial breast radiation can be given either from the outside, the way that classic radiation is delivered, or it can be given by inserting radioactive material into the cavity that is left after the primary breast cancer has been removed. The potential advantage of partial breast radiation is that less normal tissue is exposed to radiation. However, this approach is relatively new and it is not clear that it is as safe or as effective as classic radiation. Prospective randomized clinical trials comparing the two methods are now underway.

Outside of the U.S., such as Canada and the U.K., both whole breast and partial breast irradiation is given over a shorter time periods, from 3-4 weeks, to even just a few days. This “short-course” radiation could be preferable, since it saves time for the patient and resources for the medical community. Large randomized trials of whole breast irradiation given in the classic fashion or short-course suggest that the latter is as safe and effective at the former. At present, it has not been widely adopted in the U.S., mainly out of concern that followup may not be sufficiently long to be certain that the efficacy and cosmetic outcomes are not worse. Short course, partial breast radiation is still under investigation.

If a patient has a mastectomy, she may still need radiation. Prospective randomized trials have demonstrated that radiation to the remaining chest wall tissue reduces the chances of recurrence in that area (called “local recurrence”) by 60-75% of whatever the initial risk would have been. These same trials also showed a 25-30% reduction of systemic metastases in those patients who received chest wall radiation, and even longer survival. Therefore, it is common practice to recommend radiation to patients with a high risk of local recurrence: larger tumors (>5cm), positive margins in the mastectomy specimen, and multiple (4 or more) positive axillary lymph nodes. Most doctors agree that radiation should not be given to women with small tumors (<2cm), negative margins, and negative nodes. There is controversy about whether radiation should or should not be given to women with either 2-5cm tumors or 1-3 positive nodes. Women who have had inflammatory breast cancer are always treated with radiation after mastectomy. see more...

Examination of the axillary lymph nodes10, 11{Veronesi, 2003 #7858}

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.
At the time of primary breast surgery, most women have some sort of evaluation of their axillary nodes, to determine whether the cancer has spread there. This is done for several reasons, mostly related to determination of prognosis and subsequent direction of therapy. For example, most women who have positive axillary lymph nodes will receive radiation therapy to that area after surgery, while those with negative axillary lymph nodes may not. Likewise, systemic therapy decisions are often based on the presence or absence of lymph node involvement. As noted, Halsted and his followers believed that radical dissection of the axilla was an important component of breast cancer treatment, and women often had 50 to 60, or more, lymph nodes removed at the time of mastectomy. These surgeries were frequently followed by horrible complications, including massive swelling of the arm on that side because the normal drainage patterns from the arm were disrupted (this condition is called “lymphedema”). In the 1980s, data suggested that such radical dissections were not needed, and so only 10-15 lymph nodes were removed or “sampled.” Since the mid-1990s, several studies, and even a few prospective randomized trials, have demonstrated that just removing the first lymph node that drains the breast, called the “sentinel node,” may be sufficient (note: sometimes there are a few sentinel lymph nodes rather than just one, and they are all removed). If the sentinel node does not have cancer in it, it is very unlikely that any of the other axillary lymph nodes are positive, and so there is no reason to remove them. If the sentinel node is positive, the standard of care at this time is to proceed with axillary sampling (10-15 extra nodes) to determine the number of involved lymph nodes. There is even controversy about the benefit of taking out positive nodes. Some studies suggest that removal of positive nodes decreases the risk of subsequent recurrences in the axilla, while others suggest that radiation can replace surgery, and that long-term survival is not affected. However, the current standard of care for a woman with a positive axillary lymph node is further axillary lymph node resection.

Primary Treatment of Breast Cancer

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Primary Surgery8, 9. For women with stage I-III breast cancer, treatment of the primary cancer is of paramount importance. Beginning in the late 1890s, led by Dr. William Halsted and others,surgeons developed the theory that breast cancer spread in a logical fashion from the breast to the surrounding lymph nodes and then, after a period of time, to the rest of the body. Therefore, they presumed that the more local treatment that was applied, the more likely the patient would be cured. This theory led to the “Halsted Radical Mastectomy,” in which not only the breast but underlying muscle tissue were removed, as well as most if not all of the lymph nodes in the axilla. Later, radiation to the chest wall was added to augment the radical mastectomy.

In the 1940s and 1950s, doctors began to question the Halsted theory, and wondered if less aggressive local therapy, such as doing less surgery and/or not giving radiation, might be as effective as the Halsted Radical Mastectomy followed by chest wall radiation. Prospective randomized clinical trials over the ensuing 3 decades demonstrated that for approximately 60% of women with stage I-III breast cancer, performing breast “conserving” therapy works just as well as doing a mastectomy. Follow-up of these studies for more than 30 years confirms that long-term survival for women treated with breast conserving therapy is the same, or even better, than those who had a mastectomy. Breast conserving therapy involves removing the primary cancer from the breast (also called a “lumpectomy,” “wide excision,” “partial mastectomy,” or “quadrantectomy”) while leaving the rest of the breast intact. Breast conserving therapy is usually delivered as complete removal of the cancer followed by radiation to the breast. However, the value of the radiation has been questioned. Prospective randomized clinical trials of breast conserving surgery with or without radiation were found to result in an unacceptably high rate of recurrences in the breast. Therefore, currently, for most women, breast conserving treatment involves both surgery and radiation. There is at least one prospective randomized clinical trial that suggests that the radiation might not be needed in older (>65 years) women with ER positive and node negative breast cancers that are less than 2cm, but many doctors are not willing to eliminate the radiation even for this group of women until followup in this trial is much longer.

Still, there are some patients for whom mastectomy is a better treatment option. Doctors have found that if the primary tumor cannot be completely excised, the risk of having the cancer come back in the breast is unacceptably high, even with radiation after the surgery. Thus, women with large tumors and especially small breasts usually are better treated with mastectomy, since a complete excision requires removal of most of the breast anyway. Some of these women can have breast conserving treatment if they receive systemic treatment first, to shrink the cancer. This will be discussed in greater detail below. Other reasons to perform a mastectomy instead of breast conserving therapy include finding cancer at the edge of the excised tissue (this is called a positive margin), and if there are multiple cancers in the same breast, either as discrete separate cancers or evidence that the cancer is in many places. A common reason for recommending mastectomy is evidence of wide-spread DCIS, which can be presumed by mammographic finding of worrisome calcification throughout the breast once a tissue diagnosis of DCIS is made.

Most doctors also recommend mastectomy for women who initially are found to have inflammatory breast cancer, which is a special type of cancer that makes the skin of the breast look red (or “inflammatory.”). This kind of cancer is especially aggressive, Efforts at breast preservation in women with inflammatory breast cancer (often called “IBD”) have resulted in very high risks of local recurrence, so these patients are usually treated with mastectomy and radiation to their remaining chest wall and surrounding lymph nodes. Finally, there are some women for whom radiation is dangerous, and therefore they are better served with mastectomy. These include women with certain skin conditions, such as systemic lupus erythematosus, and women who have previously had radiation to the breast. The latter is most often seen in women who have had been treated for Hodgkin’s disease with radiation to their chest, or women with a prior breast cancer who were treated with breast conserving therapy.

Treatment of breast cancer

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It is helpful to think of breast cancer as a continuum from what is often termed “early” breast cancer to “advanced” or “metastatic.” Early breast cancer usually implies that the cancer is only detectable in the breast and surrounding lymph nodes, particularly in the axilla (the arm-pit). Doctors have divided early breast cancer into three stages, I, II, and III, so that they can communicate more readily and consistently with each other in a type of short-hand (See Table 3 for a brief description of the so-called TNM staging system, which is based on the size of the primary Tumor (T), the status of the axillary lymph Nodes (N), and whether there are or are not distant Metastases). In stage I breast cancer, the actual cancer in the breast (called the “primary” cancer) is small (less than 2 centimeters [cm]) and no cancer can be found in the axillary lymph nodes. Stage II primary cancers are either bigger (2-5 cm) and/or there is some involvement of the axillary lymph nodes. Stage III breast cancers are larger than 5 cm, have extensive axillary nodal involvement, and/or have certain worrisome findings on physical examination, such as redness, nodules, or ulceration of the skin, or suspicion the cancer is fixed to the muscle and bones beneath the cancer site. If the cancer can be found outside the breast and axillary lymph nodes, it is called metastatic, which is designated stage IV. Metastatic breast cancer is most often found in the bones, liver, lung, or lymph nodes outside the axilla, although it can occur in any organ. Even though it is growing in these organs, it is still considered breast cancer; when breast cancer spreads to the bone, for example, it is not bone cancer, so its treatment follows breast cancer protocols, which are different from primary bone cancer protocols.

These days, due in great part to intensive screening programs in the US and other developed countries, most patients are diagnosed with stage I-III disease. Only 5% of patients present with metastatic breast cancer at diagnosis. The odds of developing metastatic, or stage IV, breast cancer over the next 5-10 years after diagnosis of breast cancer are directly linked to the initial stage. In other words, although at time of diagnosis we cannot find metastatic cancer in other organs, very small deposits of cells (called micro-metastases) must have already left the primary cancer and spread to these sites.

Breast cancer is not one disease. Rather, there are several types of breast cancers, and these can be distinguished by a pathologist looking at the cancer under a microscope and by special testing of the cancer. Breast cancer starts in the milk glands, or ducts, and often remains confined to these ducts without any evidence of invading surrounding normal tissue. This kind of breast cancer is called intra-ductal breast cancer, or more commonly ductal cancer in situ (DCIS), which means it has stayed in the place it started. DCIS is really a pre-malignant condition, since if that is all a patient has, there is little or no chance the cancer has sent out micrometastases. If the cancer has broken out of the duct, it is called “invasive” or “infiltrating” cancer. This is the kind of cancer that is able to get into the lymph and blood vessels of the breast and travel to other sites, ultimately causing metastases.

Pathologists can also provide an estimate of how likely it is that an invasive cancer may have spread. One way is to determine if the cancer has spread to the axillary lymph nodes or not. We know that a patient with positive axillary lymph nodes has about twice the risk of developing subsequent detectable metastases than a patient with negative lymph nodes. The likelihood of developing metastases is called “prognosis.” The size of the tumor is also prognostic (hence the importance of size in the staging system discussed above), as is the tumor grade. Tumor grade is determined by an experienced pathologist who can tell under the microscope if the cancer looks like it is likely to be well or poorly behaved. Grading is based on three components: 1) does the cancer cell nucleus look bad; 2) are the cancer cells trying to make glands (worse prognosis cancers don’t make glands; rather the cells just organize in sheets); and 3) how many of the cancer cells are dividing within the microscopic field (worse cancers are dividing more rapidly). Grade is provided as I (favorable), II (intermediate) and III (poor). In addition, there are a few so-called special types of breast cancers that seem to have a particularly good prognosis, including tubular, mucinous, and colloid cancers. Additional testing of the cancer can also help to determine prognosis. Cancers that make estrogen and progesterone receptor are less like to cause metastases, especially in the first several years after diagnosis, but HER-2 positive cancers have a worse prognosis.

There are fundamentally two types of treatment for breast cancers: 1) Local treatments, which are strategies that only treat the cancer in a single region of the body, such as the primary site; and 2) systemic treatments, which are usually given orally or intravenously and go all through a patient’s “system.” Local treatments include surgery and radiation, and occasionally other locally-applied therapies such as heat therapy. Systemic treatments include anti-estrogen treatments, chemotherapy, and more recently treatments directed towards the HER-2 molecule and treatments directed towards blocking new blood vessel growth, called angiogenesis inhibitors. Overall treatment of any patient with breast cancer often requires doctors trained in the three different methods of therapy: surgeons, radiation oncologists, and medical oncologists-this type of approach is called “multi-disciplinary treatment.”

Screening for Breast Cancer

2008-08-19T16:24:00.000-07:00

Screening for Breast Cancer6, 7
There is no other cancer for which screening has been as carefully studied as breast cancer. Beginning in the late 1960s, nine prospective randomized clinical trials, involving over 100,000 women, have examined whether screening mammography, with or without a clinical breast examination by a trained professional, decreases the risk of dying of breast cancer. Of course, screening will not prevent a new breast cancer. Rather, these studies were performed based on the concept that early detection of an existing cancer results in earlier, and therefore more effective, treatment. Initially, early treatment involved solely treating the breast with surgery and possible radiation. These are called “local treatments,” meaning they only treat the local area where the cancer began. On the other hand, “systemic” treatments, such as anti-estrogen therapy, chemotherapy, and more recently anti-HER-2 therapies, go throughout the body (all through the “system”). Several prospective, randomized, controlled trials (PRCTs) have demonstrated that early application of these treatments is much more effective in preventing mortality than waiting until the cancer metastasizes outside of the breast, such as to the bones, lung, or liver. Several studies have shown that we rarely, if ever, cure patients with metastatic breast cancer, so early detection and treatment are very important.

The results of the nine PRCTs of screening mammography have generated considerable controversy through the years. Although most have demonstrated mortality reductions for those women who are screened, not all have. However, when all of the studies are pooled together, it appears that routine screening reduces breast cancer mortality in women over 50 (those most likely to get it) by approximately one-quarter to one-third. However, in many respects, these studies were over-interpreted by well-meaning doctors and lay persons to mean that screening would eliminate breast cancer deaths, which is not the case. They have also been cited to recommend that every woman should be screened-even young women less than 40 years. Other scientists have said that the “positive” studies – those that showed a benefit to screening -- were not well done, and that careful evaluation fails to demonstrate any benefit.

As of this time, much of this controversy has been laid to rest in standard clinical practice in developed countries in which breast cancer is a major health risk. In general, most expert panels that make recommendations for doctors suggest that women should begin screening mammography in their 40s and continue it until at least 70 years of age, and perhaps longer, if they are otherwise healthy and treating breast cancer, if they developed it,would be rational.

Regardless, mammography is not perfect, by any means. As noted, screening studies have only demonstrated a reduction in mortality of 25-35%. This implies that 65-75% of women who die of breast cancer will do so in spite of screening. Screening mammography only detects approximately 80-90% of all cancers; in other words, it misses around 10-20%. It is also frequently falsely positive. Up to 75% of “positive” mammograms (positive means that an abnormality is found that requires a biopsy) are not cancer.

Can we do better than screening mammography? No single modality has been shown to be better than mammography. Breast ultrasonography is widely used to help define abnormal mammograms and make them more specific, thus decreasing unnecessary biopsies. However, routine screening ultra-sonography in women without a mammographic finding has not been found to be very helpful. Recently, magnetic resonance imaging (MRI) of the breast has been intensively studied and has resulted in considerable controversy. There is no question that breast MRI is more sensitive than mammography, detecting 90-95% of all cancers. However, several (but not all) studies have demonstrated that screening MRI is less specific, so that it detects more abnormalities that require biopsy but are not cancer. MRI is also much more expensive than mammography. Currently, it seems reasonable to perform routine screening MRI in women who are otherwise considering prophylactic mastectomy but are not ready to do so, and in women with particularly dense breasts for whom mammography is notoriously insensitive.

Many other modalities to screen for breast cancer have been studied or proposed. However, none has been put to the kind of testing that mammography has, in particular PRCTs looking to see if breast cancer mortality is reduced. Many of these are like MRI-- more sensitive, but without an indication of specificity, such that using them turns up more false positive results. This may cause more harm than good by resulting in unnecessary surgeries and anxieties.

Prevention of Breast Cancer

2008-08-19T16:20:00.002-07:00

Understanding the cause and risks of breast cancer might lead to strategies to prevent it. Unfortunately, as noted, there is no single common cause of breast cancer that can be altered, as there is with lung cancer, and there are no known life-style changes that have been proven to lower breast cancer risk. Nonetheless, there are some strategies that have been shown to be effective.

Prophylactic Surgery2, 3. Prophylactic surgical removal of unaffected breast tissue (prophylactic mastectomy) appears to reduce the risk of getting a new breast cancer considerably. Due to ethical concerns, there has never been a prospective randomized clinical trial asking whether removal of breasts from otherwise normal women actually prevents breast cancer. However, retrospective and prospective monitoring studies do suggest that this is the case. This statement seems intuitively obvious, but it must be understood that the breasts are not encapsulated organs, like the kidneys, and breast tissue is diffusely distributed under the skin. Therefore, except for the most aggressive surgeries, most prophylactic mastectomies leave behind some breast tissue, which can always become malignant. Nonetheless, these studies show that prophylactic mastectomies appear to reduce the risk of getting a new breast cancer by almost 90% of whatever a woman’s risk was before the surgery. These same studies suggest breast cancer mortality is also decreased by about the same amount.

For most women, prophylactic mastectomy is unacceptable, and it is not recommended by most surgeons except for those patients with very high “genetic” risks, (in other words, women who are BRCA1 or 2 “positive”). Indeed, for a woman with average or slightly elevated risk, the adverse cosmetic and emotional aspects of this aggressive approach outweigh the small potential benefit.

Disruption of the estrogen/estrogen receptor system4, 5. As noted, approximately two-thirds of all new breast cancers appear to be driven by estrogen binding, and activation of the estrogen receptor. It has been known for years that young women with either natural or surgical premature menopause have lower risks of breast cancer than women whose menopause occurs around 50 years. However, as with prophylactic breast removal, prophylactic surgical removal of a young woman’s ovaries is associated with substantial social, sexual, and emotional difficulty. Of course, it ends any prospects of fertility. However, even if a woman has elected not to have any more babies, early menopause (less than 40 years) also appears to increase the risk of non-breast cancer medical problems, such as osteoporosis and cardiovascular disease. In fact, a recently published study from the Mayo Clinic demonstrated that woman who had their ovaries removed before age 35 had shorter life expectancy than those who went on to have natural menopause.

Rather than surgery, women can also use medical means to interrupt the estrogen/ER system. This strategy has become known as “chemoprevention.” Chemoprevention should not be confused with “chemotherapy,” which is used to treat established breast cancers after they are diagnosed, and will be discussed later. The most widely studied approach so far is the use of medicines that bind to the ER, just like estrogens. These medicines are called “Selective Estrogen Receptor Modulators” (or “SERMs” for short). Tamoxifen (Novadex™) is the oldest and most widely used of these. As we will discuss below, for the last 40 years, tamoxifen has been the mainstay of treatment of women with breast cancers that make ER. Several large, prospective randomized clinical trials (the best kind of studies) have shown that daily tamoxifen for five years reduces the risk of getting a new breast cancer by nearly one-half in women who are at moderately high risk for, but who have never had, breast cancer. Not surprisingly, tamoxifen only prevents those cancers that need estrogen (ER “positive”) and does not affect the incidence of ER negative cancers.

SERMs, such as tamoxifen, are odd medicines, reacting different ways in different cells. As a general matter, they enter all cells, but they will affect those cells that make estrogen receptor. In such cells (ER positive cells), SERMS bind the ER, so they prevent estrogen from doing so. The ER, now bound to the SERM, goes to the nucleus of the cell just as if it were bound to estrogen. In some tissues, like breast and brain, the ER-SERM combination prevents the cell from functioning, in other words in these tissues the SERM is “anti-estrogenic.” This is why tamoxifen works against ER positive breast cancers. Since the same effect occurs in the part of the brain where body temperature is controlled, and since estrogen seems to stabilize body temperature, the anti-estrogenic effects of tamoxifen frequently cause women to have hot flashes.

However, in other tissues that also need estrogen, like bone, liver, and uterus (the womb), SERMS can actually act like estrogen! Thus, tamoxifen prevents osteoporosis (bone thinning) just like estrogen does, and, like estrogen, causes the liver to make too much of the proteins that cause blood clotting. Also like estrogen, tamoxifen causes the lining of the uterus (called the endometrium) to expand, and can even cause cancer of that tissue. Women who take tamoxifen (or for that matter, estrogen, as well) are more likely to have blood clots and also to develop uterine cancers, although not very much more likely.

Scientists have tried to identify other SERMs that might be preferable to tamoxifen. One of these, raloxifen (Evista®), has been compared directly to tamoxifen as a preventive agent in a prospective randomized clinical trial of higher risk women. In this study, raloxifene was a little less effective in preventing cancers, but also a little less likely to cause blood clots. Raloxifene does not appear to affect the uterus at all, so it does not increase the risk of endometrial cancer. Raloxifene has already been proven to prevent osteoporosis compared to placebo, and it is approved by the FDA for this use. It is not known whether raloxifene is better or worse than tamoxifen for this use.

So far, widespread acceptance of either of these agents to prevent breast cancer has been limited, in part due to the annoying side effects (like hot flashes and sexual difficulties) and occasional life-threatening toxicities (like blood clots or uterine cancers). It has not been shown that use of these agents results in reduction in mortality, partly because even “high risk” women, other than those few with genetic risk, are not terribly likely to die of breast cancer over a 5-10 year period of time, and perhaps because SERMs are mostly preventing the cancers we are most likely to cure anyway.

These considerations highlight that we need better ways to medically prevent breast cancer. Some research on preventive mechanisms has come from observations of postmenopausal women who have been diagnosed with ER positive breast cancer. In this group, several prospective randomized clinical trials have shown that completely preventing estrogen production is slightly more effective than tamoxifen in preventing a recurrence of that cancer (this strategy will be discussed below in TREATMENT OF BREAST CANCER: Systemic Therapy). Even postmenopausal women make some estrogen, but not from their ovaries, as do younger women. Rather, older women make a precursor of estrogen in their adrenal glands (the same glands that make adrenaline), and this precursor is converted to estrogen in other cells (mostly fat cells). This is the equivalent of an oil well (the adrenal glands) making crude oil and the refineries (the fat cells) converting it into gasoline. This conversion is performed by a protein in the fat cells called an aromatase. Three drugs that inhibit aromatase function have been approved by the FDA to treat women with established breast cancer. In addition to preventing recurrences in women who have ER positive breast cancers, all three appear to also prevent new breast cancers in those women who have another breast. Prospective randomized clinical trials comparing these to placebo or to a SERM to prevent breast cancer in high risk women who have never had breast cancer are either underway or planned. Since these agents are pure anti-estrogens, they have some of the same but also different side effects and toxicities. Like the SERMs, they cause hot flashes and sexual difficulties. However, they actually increase the risk of osteoporosis, while not causing blood clots or uterine cancers. They also cause a common complaint of joint aches and pains, which in approximately 10-15% of women can be quite severe. It is not recommended that a woman without breast cancer take any of these aromatase inhibitors for prevention, outside of a clinical trial at this time.

We still do not have any good, safe, and effective measures, other than surgery, to prevent ER negative cancers. This is an area of active research in many laboratories, but currently nothing has been very promising in clinical trials.

Who gets Breast Cancer (Risk)?

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The most important risk factors for developing breast cancer are being a woman and being older (over 50). More than 75% of breast cancers occur in this group of people. While breast cancer does occur in men, it is quite rare (about 100 fold less common than in women). Likewise, although 25% of all breast cancers do occur in women less than 50 years, most of these occur in women 40-50 years old. Breast cancer in women less than 40 is certainly seen, and the diagnosis must be considered in a young woman with a breast abnormality, but it is really not very common. In fact, other than being a woman over 50, known risk factors like family history and benign breast conditions can only be found in about 25% of all patients with breast cancer. This is called “attributable” risk (meaning that, of all the patients who have the disease, what percentage actually have the risk factor?). A great example of a very strongly-associated attributable risk factor is smoking for lung cancer. More than 90% of all patients with lung cancer have been or are smokers. A second kind of risk is called “relative risk.” In other words, if you have the risk factor, how much more likely are you to get the disease than someone without it. We have already discussed being female vs. male for breast cancer, for which there is a very high relative risk (more than 100-fold). Returning to lung cancer, subjects who have smoked for ten years or more have a 10-fold or higher relative risk of developing the disease than those who have not smoked. Most of the known risk factors for breast cancer, especially those with reasonably high attributable risks, such as reproductive history, only have relative risks of 2-fold or less. The final kind of risk is called “absolute” risk -- in other words, if you have the risk factor, how likely are you to actually get breast cancer over some period of time, such as the next five, 10, or 15 years? With a few exceptions, none of the known risk factors, even when combined into an index that takes several risks together, results in a very high absolute risk over a relatively short period of time. For example, Dr. Mitchell Gail and colleagues have created such an index to determine risk for individual women. Even those with several factors often only have an absolute risk of 3-5% over the succeeding five years.

Why determine these kinds of risks? First, they may provide insight for future research. For example, the observation that women are much more likely to get breast cancer than men led to the thought that the disease must be associated with female reproductive hormones, like estrogen and progesterone, and this observation has further led to remarkable clinical advances that have resulted in prevention and treatment of the disease. Second, if strategies to prevent and/or screen for the disease are known to be effective, they will be much more efficiently applied to those most likely to get it. In this case, attributable risks are the most important, to decide which populations should be included. For example, we don’t recommend screening mammograms for men, since such a small percentage of breast cancers occurs in men. Furthermore, even if his relative risk is elevated, for example by having a mother with breast cancer, a man’s absolute risk of developing breast cancer is still so low that it would essentially be a waste of time and resources. Finally, a patient’s absolute risk is the most powerful determinant of whether she should or should not participate in screening or treatment strategies personally, since one does not want to expose one’s self to the costs and toxicities of a given strategy if there is a very small, or no, chance of getting the disease. Incidentally, a version of the program developed by Dr. Gail and colleagues to calculate an individual’s risk of getting breast cancer over a five year period of time is available online at http://www.cancer.gov/bcrisktool/about-tool.asp and you can estimate your own chances of getting breast cancer if you’d like.

The risk of breast cancer is increased if a woman takes estrogen therapy, especially if it is associated with progesterone. A recently conducted prospective study in which postmenopausal women were randomly assigned to either take estrogen and progesterone therapy or neither was terminated early due, in part, to an excess of breast cancers in the treated group, an observation that is consistent with prior epidemiologic studies. When the results of this study were announced in 2003, the use of combined estrogen and progesterone therapy, which was widespread up to then, dropped precipitously in our society. In the last couple of years, the overall incidence of breast cancer has dropped in the U.S., presumably due to women discontinuing estrogen and progesterone use.

It is not clear if estrogen therapy alone increases the risk of breast cancer. Indeed, in a companion prospective trial to the one discussed above, women who had had a hysterectomy were randomly assigned to estrogen therapy alone or not. In the first study, progesterone had been added because it has been known for years that estrogen increases the risk of uterine cancer (cancer of the lining of the womb, which is also called the endometrium). Obviously, because the women in the second study had had their wombs removed, the risk protection from uterine cancer that the progesterone conferred was not felt to be needed. In this second trial, an increase in breast cancer has not been seen, suggesting that perhaps the increased risk in the first study was due to the progesterone, either itself, or perhaps because it couples adversely with estrogen.

It is not clear whether oral contraceptives (birth control pills) do or do not increase the risk of breast cancer. No trial has ever been conducted in which women are randomly assigned to get birth control pills or not, and the epidemiologic studies of this issue have been mixed. They are complicated to do because oral contraceptives come in many forms, with different doses of estrogen, with or without other hormones like progesterone, and women have taken them for different periods of time and in different phases of their lives. Overall, it seems reasonable to suggest that the benefits of birth control pills, with regard to preventing unwanted pregnancies, outweigh whatever small risk they might cause for breast cancer.

We don’t know why or how estrogen and progesterone cause a normal breast epithelial cell to become a cancer cell. Laboratory studies clearly show that these hormones are necessary and increase the growth of most, but not all, normal and cancerous breast cells. Indeed, doctors routinely measure the estrogen receptor in breast cancer tissue. The estrogen receptor (designated ER) permits the breast cell to pull estrogen out of the blood and use it to function. Anti-estrogenic therapy, which is the mainstay of treatment of breast cancer, only works in those women whose cancers make ER, as discussed in greater detail below. However, in laboratory studies, neither estrogen nor progesterone alone will make a normal breast cell become malignant, and many women have taken estrogen for years and do not develop breast cancer. Therefore, scientists believe that there must be an interaction between an inherent susceptibility to cancer for individual women and other, non-hormonal factors.

No one has identified any other definitive causes of breast cancer. Several different environmental and dietary factors have been suggested and heavily studied, but none has been shown to be a causative culprit. It is true that obese women, and women who drink moderate to large amounts of alcohol have a higher risk of breast cancer, but it is not known if these are causative or just related to something else that causes the cancer. Therefore there are no clear life-style changes that a woman can make to substantially reduce her risk of breast cancer (as there is for lung cancer: DO NOT smoke, or if you do, STOP). It is conceivable that delaying menarche (when a girl begins to menstruate) to an older age or electing to have a first full-term pregnancy at a young age (less than 21 years) will decrease risk. However, these are not terribly practical strategies and will only modestly reduce the risk for breast cancer.

Inherited, Genetic Risk1. Obviously, only a few women with exactly the same apparent risk factors will actually get breast cancer. The variability of who does or does not get breast cancer suggests that there may be factors that women inherit that make them more susceptible. For example, we know that other than being a woman over 50 years old, the most common risk factors are either having a family history or having had breast cancer yourself, suggesting these women are more susceptible and may have inherited the same risk factor that their family members inherited. In fact, scientists have worked very hard to identify abnormalities in genes that a woman has inherited from her mother or father that places her at high risk. About 15 years ago, two such genes were identified. They are called BRCA 1 and 2. When these function normally, BRCA1 and 2 are tumor suppressor genes. Everyone has two copies of these genes in their cells; one copy comes from your mother and the other from your father. For most women BRCA1 and 2 appear to function by preventing normal cells that make mistakes during division from becoming malignant. Normally, in all cell division, mistakes are occasionally made in many genes within the cell. BRCA1 and 2 appear to function by fixing these mistakes after the cell divides so they are not passed on in the next division, much like a spellchecker program finds and fixes mistakes in a wordprocessing manuscript. Mistakes also occur in BRCA1 and 2 in normal division. It appears very unlikely that mistakes occur in both copies of BRCA1 or 2 at the same time. Thus, the remaining normal copy can go about its business fixing other genes while the “broken” copy of BRCA1 or 2 is fixed, itself. In this case, the other genes all get fixed, and before the cell divides, it has been returned to having two normal copies of BRCA1 or 2. This situation is analogous to being born with two good legs; if one is fractured, you can walk with a crutch until it is healed, and then you are fine.

In a few families, one or the other copies of the BRCA 1 or2 gene is abnormal to begin with in every cell. Therefore, only one copy is working. This is fine for most of the time, but if the only normal copy of BRCA1 or 2 is damaged, there is no “backup” second copy (since it never worked). In this case, cells that in the ordinary course may sustain damage to other genes are in danger of having no repair backup, and becoming malignant. Using our “leg” analogy, if you are born with only one good leg, you can walk with help, but if that leg is damaged, you fall down.

BRCA1 and 2, if abnormal, confer enormous relative risk for the populations that have them (10-fold or higher), and absolute risk for those affected individuals. Up to 60% or more of women who are born with abnormal BRCA1 or 2 genes will develop breast cancer by the time they are 60 years old, and they are much more likely to get the cancer at an early age and more than once. Furthermore, they are also at risk for some other cancers, especially ovarian cancer. Incidentally, these women are often said to be “positive” for these genes, but of course what we really mean is that they are “positive” for having abnormal copies of the genes. However, BRCA 1 and 2 are very low attributable risk genes. Only about 5% of women with breast cancer are found to have abnormal inherited copies of these genes, and the rest are born with normal copies.

Should you be tested to see if you have abnormal BRCA 1 or 2 genes? For most women, the answer is no. The odds of the average woman being abnormal are quite low, and although the test only requires a simple blood draw, it is technically difficult and expensive to perform. Furthermore, on occasion it provides false positive testing, or more commonly the results are equivocal (meaning that it finds unusual changes, but the clinical significance of these is unknowns). Therefore, panels of experts have recommend that testing only be performed for those women most likely to be positive. These include one or more of the following:
Personal age <40 years at time of breast cancer diagnosis
Ashkenazi Jewish Heritage
Personal or first or second degree relative with history of ovarian cancer
First degree relative with history of breast cancer diagnosed before age 50
Two or more first or second degree relatives with history of breast cancer at any age
Personal or any first or second degree relative with bilateral breast cancer
History of breast cancer in male relative

Scientists have worked hard to identify other genes that a woman might inherit that increases her susceptibility to breast cancer. It is very obvious that there are no other genes that, if abnormal, have the kind of strength that BRCA1 and 2 have to cause a woman to develop breast cancer. Rather, we now believe it is likely that most women who get breast cancer have two or more genetic abnormalities (more precisely put, differences from other unaffected women rather than an abnormality) that by themselves don’t do much. However, when present in the same individual who is then exposed sufficiently often to external factors that might cause the disease, she is more likely to get breast cancer.

The hunt for these genes has been exceedingly frustrating. Many “candidate” genes (that is, knowing what they do in the normal setting that suggests that they might, logically, result in cancer if abnormal) have simply not panned out as risk factors in epidemiologic studies. However, a recent reported study regarding a mammoth effort by many highly experienced experts in the field has suggested that there might be four genes that are new “candidates.” Intensive study of these candidates will be the focus of future research.

What Causes Breast Cancer?

2008-08-19T16:19:00.000-07:00

No one knows for sure what exactly causes a normal cell to become breast cancer, or for that matter, any cancer. We do know that normal cells have built-in controls that permit them to divide sufficiently to maintain normal healthy tissue, but not more than is necessary. Normal cells are also unable to leave where they are supposed to do their normal job (such as in the breast duct) and travel to other sites. Cancer cells lose these internal controls; they divide too much and they are able to travel to other sites and grow (metastases). Over the last two decades, we have seen remarkable breakthroughs in understanding these processes. For example, all of our cells have genes that maintain these normal controls on cell growth, invasion, and spread. Indeed, if a cell has been irrevocably damaged during its normal division, there are even genetic programs that cause that cell to kill itself (this process is called “apoptosis”). These genes are called “tumor suppressor genes,” and we know that one cause of cancer is damage or deletion of one or more of these genes, so the rest of the genes in the cell go haywire. We also know that certain genes that are necessary for normal cell division, growth, and movement can develop mutations that result in uncontrolled activation, so that a cell loses its normal control. When these occur, these genes are called “oncogenes.”

For most patients, development of cancer appears to be a combination of a genetic propensity to develop cancer (for example, by inheriting abnormal tumor suppressor genes that do not do their job as well as normal ones do in other people), and exposure to environmental factors that induce or enhance the changes that result in cancer. Unlike lung cancer, for which smoking is a compelling causative factor, there have been no clearly identifiable causes for breast cancer. However, decades of epidemiologic research have demonstrated that breast cancer is clearly associated with female reproductive hormones, like estrogen and progesterone, either when taken as medicine or when made by the patient herself. For example, although men do get breast cancer, their risk is nearly 100-fold less than that for women. The risk for breast cancer is about two-fold higher for women who start their periods young (less than 13 years old) and who delay their first full term pregnancy into their 30s, while women who have a premature menopause appear to have a lower risk than those whose menopause extends into their 50s. We also know that estrogen therapy, especially when combined with progesterone, increases a woman’s risk of getting breast cancer. Ongoing research is addressing other possible causes, but so far none has been discovered.

No one knows for sure why estrogen causes breast cancer. However, over 100 years of clinical and laboratory research has demonstrated that about 65-75% of breast cancers require estrogen to live, spread, and grow. These types of breast cancer contain a molecule inside their cells called the “estrogen receptor.” Estrogen itself, either made by a woman or taken as medicine, floats through the bloodstream and diffuses (enters) into cells. Those cells that have the estrogen receptor inside of them capture the estrogen and then transmit a “go” signal to the nucleus. This system is a bit like an automobile that needs gasoline. You can think of the cell as the automobile, estrogen as gasoline, the estrogen receptor as a gas tank, and the nucleus of the cell as the engine. Estrogen receptor (called ER, for short), and its cousin, progesterone receptor (called PR) can be easily measured in breast cancer tissue, and it is standard practice to do so.

What makes breast cancers that do not need estrogen grow? Other factors have been found, the most important of which is a molecule called HER-2 (for Human Epithelial Receptor-2). About 20% of breast cancers make too much HER-2, which sits on the surface of the cell and controls and transmits signals from outside the cell down to the nucleus. Let’s continue with our automobile analogy. You might think of HER-2 as a solar panel. A car might get some or all of its energy from the sun, but it would need a solar panel to do so (don’t get confused, though: breast cancer has nothing to do with sun exposure, this is just an illustration). Most breast cancers that are positive for estrogen receptor do not make HER2, but some do. More estrogen receptor negative breast cancers make HER2. Regardless, breast cancers that make HER-2 are more aggressive than those that do not. There are many breast cancers (maybe 25%) that do not make ER, PR, or HER2; lately, these have been designated as “triple negative” cancers, in part because there is no specific therapy for them as there is for ER and HER-2.

What is Breast Cancer?

2008-08-19T16:18:00.000-07:00

The usual breast cancer begins in the cells that line the milk glands of the breast. These are called epithelial cells. The cancer may arise from the glands that actually initiate the milk production, called the “lobules,” or more commonly it may arise from the cells that line the ducts that normally transport the milk from the lobules to the nipple. In fact, 90% of breast cancers are felt to be ductal, while approximately 5% are lobular, and the rest are considered to have begun in the duct but have unusual appearances under the microscope and are called “special types.” These special types include “tubular,” “mucinous,” “colloid” and “medullary” breast cancers.

In general, ductal and lobular cancers have about the same prognosis, although lobular cancer has some odd characteristics that can make it harder to see on a mammogram and harder to detect when it spreads to lymph nodes. In addition, when lobular cancers spread (this process is called metastases), it often goes to unusual places in the body, like the lining of many body cavities. The special types are usually associated with very favorable prognosis.

Medullary cancers are particularly vexing. They have features under the microscope that make them appear to be very aggressive. However, if a patient has “classic” medullary cancer, her prognosis is quite good without any therapy except treatment of the cancer where it started with surgery and radiation. In contrast, if the medullary cancer is considered “atypical,” her prognosis is actually much poorer and chemotherapy is very likely to improve her long-term chance of survival.

Non-epithelial malignancies can arise in the breast, but they are very unusual. These can include sarcomas (cancers of fibrous, fat, or muscle cells) and lymphomas (cancers that arise from lymph cells). These cancers are treated as if they had arisen anywhere in the body, and those discussions are outside the scope of this review

Breast Cancer

2008-08-19T16:15:00.001-07:00

Breast Cancer is the most common lethal malignancy among women in the Western World. Approximately a quarter million American women will be diagnosed with breast cancer in 2007.

Breast Cancer is the most common lethal malignancy among women in the Western World. Approximately a quarter million American women will be diagnosed with breast cancer in 2007, and roughly 40,000 will die of it. However, remarkable scientific progress over the last four decades has led to important advances in clinical evaluation and management in several areas of breast cancer, including risk, prevention, screening, and treatment. These advances have resulted in substantially lower mortality while decreasing the adverse consequences of treatment.

Clinical Science
To fully understand much of the discussion about progress in breast cancer, it is worthwhile to take a brief digression into the importance of clinical science and how doctors make decisions. Classically, doctors have decided on a course of action for a patient based on their clinical experience or recommendations of others they perceive to be experts in the field. Over the last 10-15 years, many leaders in medicine have called for what is now termed “evidence-based” medicine, using results from scientific clinical studies to direct clinical decisions. Of course, the classic approach was based on evidence. For example, if a doctor gave penicillin to a patient with pneumonia and the patient improved, that doctor had evidence that penicillin is effective against pneumonia. However, this type of evidence is not very accurate and is not really based on the scientific method. In the scientific method, a scientist develops a hypothesis and then prospectively designs an experiment in which all conditions are controlled except a single variable, with appropriate negative controls to be certain that the observation of an effect (like the patient improving on penicillin) would not have happened anyway, or was simply due to chance alone. While we usually think of this method being used by laboratory scientists, it also pertains to clinical science.

Available evidence to guide clinical decisions has been placed into “levels” (which are really grades or scores), each of which is likely to provide a more accurate estimate of the truth of the observation than the next. For example, retrospective studies of populations (looking back) to see who did or did not get some type of disease can be compelling, but can be confounded by many variables that were not and cannot be controlled. It is clear that women in developed countries have a higher risk of breast cancer than those in agrarian and third world cultures. When one hears this, you might think of many different reasons why this is true, including dietary changes, exposure to environmental toxins, or higher rates of taking estrogen therapy. However, you might also conclude that driving expensive cars or watching color television might also be causative. This sort of clinical research is called epidemiology, and although it is valuable for developing new hypothesis, it is considered a lower level of evidence than the gold standard for clinical research: the prospective randomized clinical trial. In the latter, a group of subjects that are at risk for a particular occurrence, like developing breast cancer, are enrolled into a trial and assigned to a particular intervention (receipt of a drug or treatment) or not (often the usual standard of care medication or treatment, and sometime a placebo drug or no intervention) in a random fashion. For example, high-risk patients might be assigned to receive a drug for which preliminary, lower evidence studies have suggested a preventive role. Randomization is often done by computer, but not always.

Prospective randomized clinical trials are designed so that everyone in the study receives standard of care, but some are randomly assigned to an investigational arm that challenges the standard of care while the others are not. These trials are carefully reviewed by ethical review boards comprised of both scientists not involved in the trial as well as regular citizens from all walks of life. Once they are begun, the trials are carefully monitored to be certain that their ongoing conduct remains scientifically reasonable and ethically appropriate. Any patient who is considering being in such a trial should carefully discuss the risks and benefits of participating with his/her caregiver, and all patients who enter a clinical research study must sign a written consent form.

When completed, prospective randomized clinical trials usually provide a definitive answer regarding whether the investigational intervention is or is not preferable to standard of care. Indeed, not infrequently, several prospective randomized clinical trials addressing a similar issue are conducted by different scientists with similar ideas at the same time. If the design of these studies is sufficiently similar, the result of these studies can be combined into what is called a “meta-analysis” that, essentially, results in a “mega” study. Many clinical scientists consider these meta-analyses, or “overviews,” of many prospective randomized clinical trials to represent the highest level of evidence.

During the following discussions, I will refer to various studies and provide assessments as to the level of evidence that is available to guide doctors and patients while they make difficult clinical decisions. Fortunately, breast cancer investigators have a long and rich history of conducting prospective randomized clinical trials, dating to the 1940s, so that patients can be informed with reasonable confidence of the relative pros and cons of electing one type of clinical approach vs. another. However, of course, we still do not know all the answers, and ongoing prospective randomized clinical trials will continue to provide important answers for women at risk for, or who develop breast cancer in the future. Many studies have demonstrated that women who participate in such trials, even if they are randomly assigned to the “standard” arm, often have better outcomes than women treated in a standard fashion outside of the protocol, demonstrating that good clinical research is good clinical medicine.

Should you be in a clinical trial? This is a very personal decision. People participate in clinical trials for a number of reasons. Just by being in a trial, it is likely you will receive excellent care overall, and if you are receiving the investigational strategy, it is possible you will benefit. However, it is also possible that the investigational strategy will turn out not to be better than standard therapy, and it might even be associated with increased side effects. Most patients participate with the knowledge that regardless of the outcome of the trial, others will be helped. If the trial shows the investigational approach is better, then the next generation of patients will receive better overall treatment. If it is not, the trial will prevent the next generation from being exposed to the toxicities and cost of ineffective therapy. You should ask your doctor if there is a clinical trial available that is appropriate to your circumstances. If there is, you should read the consent form, which has been carefully written to describe the reasons behind the study and all of the potential risks and benefits of your participation, and discuss it in detail with your caregiver and your family and friends.