Does Sex Protect You Against Cancer?

Sex is more than physical pleasure: it may bring benefits on a long term. Many philosophies plead for total abstinence and preservation of the sexual energy for a prolonged life, but science comes up with another story.

In fact, many researches have showed that sex has a rather healing effect, on both psychical and physical levels. Of course, sex must be healthy, clean as on the other hand there is a wide array of sexually transmitted diseases. Frequent orgasms (about 100 per year) have been linked to an increase of 3-8 years in a person's lifespan and a decrease of death risk of 50%.

Perhaps nobody would have expected this, but sex decreases cancer rates. And in both sexes!

Researches found that sexually active women have a lower risk of developing breast cancer. When it comes to men, numerous researches have shown that a high ejaculation frequency and sexual activity are linked to a lower risk of prostate cancer later in life. A study found out that men who ejaculated 13 to 20 times monthly presented a 14% lower risk of prostate cancer than men who ejaculated on average, between 4 and 7 times monthly during most of their adult life. Those ejaculating over 21 times a month presented a 33% decreased risk of developing prostate cancer than those on the baseline.

Many cancers can be boosted by impairments of the hormonal balance, and perhaps sex and orgasm can fix this. Indeed, increased estrogen levels have been linked with higher risk of many cancers and increased testosterone levels in men has been linked to greater risk for prostate cancer.

But too much sex can be harmful for your health. In fact, over sexual partners increase the risk of infection with papillomavirus (HPV), a common genital virus, which can be transmitted even through anal and oral sex, by 8.6 times.

The human papillomavirus (HPV) is the leading cause of cervical cancer (in uterus) (95 % of the cases). Due to oral sex, HPV can provoke larynx, esophagus and oropharyngeal cancer (cancer of the throat, tonsils and back of the tongue), in a rate higher than heavy smoking or alcoholism. This virus can also provoke periungual skin, vulva, vagina, penis, perianal and anus cancer and it is also suspected to provoke breast cancer

Everything You Want to Know About Sex and Cancer

How does your sex life affect the chances of your getting cancer? Does the sensuous woman have more or less cancer than the celibate? And how about the man? Does circumcision help; and whom does it help? And what about orgasmic frequency? There is very little need to answer these questions, because an increase or decrease in cancer is not likely to deter those who are enjoying sex, nor encourage those who aren't. Nevertheless, with a "modern" book, we have to have something about sex in it. I will deal with women and men separately because, although their sexual interaction is a thing in common, the types of cancer that are related to it are not.

Cancer of the breast appears to be influenced to some degree by reproduction. It has been known for some time that there is a relatively high incidence of breast cancer among nuns, and that marriage, having children, and nursing them appears to reduce the incidence. Since marriage, having children and nursing are interrelated, it is very difficult to separate these factors. The early work suggested that long-term nursing reduced the incidence of breast cancer. This has never been substantiated, but we can still say that having children reduced the chances of getting breast cancer, and having children at a relatively early age appears to reduce the chances of getting breast cancer even more. It is also reasonably certain that having children and nursing them does not, as it does in mice, increase the incidence of breast cancer. In mice, the more pregnancy, the more breast cancer. No one has ever satisfactorily explained this discrepancy.

Cancer of the uterine cervix has its highest incidence in prostitutes, and its lowest in nuns. That ought to tell you something.

You can't win, ladies, because what increases the risk of breast cancer decreases the risk of cancer of the uterine cervix: pregnancy reduces the incidence of cancer of the breast and increases the incidence of cancer of the cervix, while celibacy increases the incidence of cancer of the breast and reduces the incidence of cancer of the cervix. You might as well do what you enjoy, because in the long haul it makes little difference in terms of cancer risk.

Cancer of the penis is very rare in circumcised men and, interestingly enough, cancer of the uterine cervix has a very low incidence in women married to circumcised men. It has not been determined whether this represents a cause and effect relationship, or whether these observations are both due to a common factor, such as a high level of marital fidelity in wives of circumcised men.

The lowest incidence of cancer of the prostate is found in Japanese men. This has been attributed to the early and regular sex habits of the Japanese male; an orgasm a day keeps the urologist away. J. D. Ferguson says that "Exemption both from baldness and gout has been credited to eunuchs since Hippocratic times. More recently it was suggested that such individuals likewise enjoy immunity from prostatic cancer. Convincing proof of this is hard to obtain, but, as yet, no instances of the disease have been reported in such circumstances. From an experimental aspect, however, there is no doubt that in domestic animals subjected to early castration, the prostate remains permanently underdeveloped, and it seems logical to suppose that a similar state in man might reduce any subsequent risk of malignant change. Despite this, it is obvious that prepubertal emasculation cannot be accounted an acceptable method of prophylaxis." Incidentally, castration is guaranteed to prevent cancer of the testicle.

There is a very very old joke that goes something like this: A salesman comes to the big city for a convention and is accosted at the train station by a woman who approaches him and says "I'm selling" and he replied "I'm buying," and they go off together. When he returns home, he finds that he has acquired gonorrhea. The following year, on his trip to the big city, he meets the same woman who says "I'm selling" and he replied "I'm buying" and again they go off together. On his return home, he finds that he has acquired syphilis. The following year he returns to the big city and meets the same woman at the station. She says "I'm selling," and he replies "What are you selling now, cancer?" Well, it looks as if this little dirty joke might well have been prophetic. A recent study, which has not been confirmed, indicates that people with cancer of the prostate tend to have had both venereal disease and a larger number of sexual partners than a control population that did not have cancer of the prostate. This appears to be a well-controlled study, but the samples are relatively small, and the conclusions drawn have to be tentative until the work has been repeated.

Some scientists have postulated that both cancer of the uterine cervix and cancer of the prostate might be caused by a herpes virus (a first cousin of the virus that causes cold sores). If this were so, one would expect some correlation between the national incidence of cancer of the uterus and the incidents of cancer of the prostate. There doesn¹t seem to be any such correlation, with a country like Australia ranking in the top ten with cancer of the prostate and the bottom ten for cancer of the uterus. South Africa ranks first in cancer of the prostate and fifteenth in cancer of the uterus; while Venezuela ranks first in cancer of the uterus and twenty-fifth in incidence of cancer of the prostate. At the present time, I know of no satisfactory explanation for these conflicting findings. If a man wanted to play it safe, he would stick to one woman. He might have less fun, but he might also have considerably less trouble.

After reading this chapter, a woman told me that she thought that she would get neither cancer of the cervix nor cancer of the breast because she had had children at an early age, nursed them all, and had remained reasonably faithful to a series of circumcised men.

In summary, it appears as if people might reduce their chances of getting cancer a bit by having frequent sexual intercourse with the same partner and having children at a reasonably early age (now, doesn't that make you happy, Doctor Ruben?). To avoid cancer of the uterine cervix, celibacy can be recommended; but that is the only thing that it has to recommend it.

Oral sex can cause throat cancer

People who have had more than five oral-sex partners in their lifetime are 250% more likely to have throat cancer than those who do not have oral sex, a new study suggests.

The researchers believe this is because oral sex may transmit human papillomavirus (HPV), the virus implicated in the majority of cervical cancers.

The new findings should encourage people to consistently use condoms during oral sex as this could protect against HPV, the team says. Other experts say that the results provide more reason for men to receive the new HPV vaccine.

Maura Gillison at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, US, and colleagues collected blood and saliva samples from the throats of 100 patients diagnosed with cancers of the tonsils or back of the throat. The scientists also took samples from 200 healthy people for comparison.

By combining the blood and saliva samples with antibody molecules, Gillison's team could tell whether a person had ever had an HPV infection.

Cancer traps
All of the study participants provided information about their sexual history, including the number of people with whom they had engaged in oral sex.

After controlling for other risk factors for throat cancer, such as drinking and smoking, the analysis revealed that people who had prior infection with HPV were 32 times as likely to have this cancer as those with no evidence of ever having the virus. And those who tested positive for a particularly aggressive strain of the virus, called HPV-16, were 58 times more likely to have throat cancer.

By comparison, either smoking or drinking increases the risk of such cancer by about threefold.

The throat cancers analysed in the new study mostly started in the "crypts" of the throat - the grooves at the base of the tonsils. This might be because the tonsil grooves trap infectious particles, suggests Mark Stoler of the University of Virginia in Charlottesville, US, who was not involved in the study.

High risk levels
The study also revealed a link between oral sex and throat cancer caused by HPV. People who had one to five oral-sex partners in their lifetime had approximately a doubled risk of throat cancer compared with those who never engaged in this activity - and those with more than five oral-sex partners had a 250% increased risk.

There was an even stronger link between oral sex and throat cancers clearly caused by HPV-16 (those tumours that tested positive for the strain). People with more than five oral sex partners had a 750% increased risk of these HPV-16-caused cancers.

"This study is important because it is putting all of the pieces together," says Gillison. "We need to add oral HPV infection to the list of risks for oral cancer," she adds.

Virus vaccine
A vaccine against several of the most aggressive strains of HPV linked to cervical cancer received approval from the US Food and Drug Administration in 2006. However the plan to vaccinate adolescent girls with this vaccine developed by Merck, called Gardasil, has received some criticism.

There have been no studies investigating whether the vaccine can also protect against throat cancer, but the new evidence linking HPV to throat cancer could lead to broader vaccination with Gardasil. "We will see a push for vaccination in men," says Stoler, who has been involved in the development of the vaccine.

Tonsil and throat cancers affect about two in every 100,000 adults in the US. The new results could promote the development of spit tests for HPV infection to help identify people at high risk for these cancers, researchers say

Cancer - renal pelvis or ureter - Overview

Alternative Names
Transitional cell cancer of the renal pelvis or ureter

Definition of Cancer - renal pelvis or ureter:
Cancer of the renal pelvis or ureter is cancer that forms in the pelvis or the tube that carries urine from the kidney to the bladder.

Causes, incidence, and risk factors:
Cancer can grow in the urine collection system, but is uncommon. As a group, renal pelvis and ureter cancers account for no more than 5% of all cancers of the kidney and upper urinary tract. They affect men more often than women and are more common in people older than 65.

Tumors of the renal pelvis and ureter are usually transitional cell cancers. Approximately 10% are squamous cell carcinomas.

The causes of this cancer are not completely known. Long-term (chronic) irritation of the kidney from harmful substances removed in the urine may be a factor. This irritation may be caused by:

•Analgesic nephropathy
•Exposure to certain dyes and chemicals used to manufacture leather goods, textiles, plastics, and rubber
•Smoking
Patients with a history of bladder cancer are also at risk.


Kidney anatomy

•Reviewed last on: 6/10/2008
•David C. Dugdale III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; and James R. Mason, MD, Oncologist, Director, Blood and Marrow Transplantation Program and Stem Cell Processing Lab, Scripps Clinic, Torrey Pines, California. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

Cancer of the ureter and renal pelvis

This information is about primary cancer of the ureter or renal pelvis. This means cancer that has started in the ureter or renal pelvis.



The ureters and the renal pelvis
Cancer of the ureter and renal pelvis
Causes
Signs and symptoms
How it is diagnosed
Further tests
Staging and grading
Treatment
Follow up
Your feelings
References
The ureters and the renal pelvis
The ureters are hollow muscular tubes that carry urine from the kidneys to the bladder. The renal pelvis is the lower part of each kidney that connects to each ureter.




Structure of the kidneys


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Cancer of the ureter and renal pelvis
Cancers affecting the ureter and renal pelvis are rare. Approximately 400 people are diagnosed with this type of cancer in the UK each year. Cancer of the ureter and renal pelvis tends to affect more men than women, and is rare under the age of 65.

The main type of cancer affecting the ureter and renal pelvis is called transitional cell carcinoma (TCC). This type of cancer develops in cells, known as transitional cells, which form the lining of the bladder, ureters and renal pelvis. Usually only one ureter or renal pelvis is affected.

Another, more common, type of cancer that can affect the kidney, is known as renal cell cancer (RCC). The tests, investigations and treatment of RCC are very different. This information is only about TCC. Our general information on kidney cancer covers the treatment of renal cell cancer.

Very rarely, other types of cancer can start in the ureter or renal pelvis. These include some types of lymphoma (a cancer that starts from the cells of the lymphatic system) and sarcoma (a cancer that develops from the supporting tissues of the body, such as muscle or cartilage).

Cancer that starts in the ureter or renal pelvis is known as primary cancer. When cancer spreads from another part of the body to the ureter it is known as secondary or metastatic cancer in the ureter or renal pelvis.



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Causes
The exact causes of cancer of the ureter and renal pelvis is unknown. It is thought that smoking may increase the risk of developing these types of cancer. People who have been exposed to certain chemicals used in dye factories and chemical industries are also at a slightly increased risk.

There may also be an increased risk in people who have papillary necrosis, a condition where parts of the kidney are damaged or have died off. Papillary necrosis can occur because of overexposure to certain painkillers, and sometimes in people who have conditions affecting the kidney, such as diabetes or repeated infections.

Cancer of the ureter and renal pelvis, like other cancers, is not infectious and so cannot be passed on to other people. It is not caused by an inherited faulty gene, so other members of your family are not likely to develop it.



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Signs and symptoms
The symptoms of cancer of the ureter and renal pelvis may include any of the following:

blood in the urine (haematuria)
passing blood clots in the urine
unexplained weight loss
having to pass urine frequently
pain when passing urine
back pain or cramps
fatigue (tiredness and lack of energy)
anaemia (if you have been passing blood in the urine for some time), but this is rare.
Sometimes the ureter may become blocked, either by cancer cells or by a blood clot. If this happens, the above symptoms may develop more quickly and may be more severe, often accompanied by a high temperature. This is known as a ureteric obstruction.

The above symptoms may be caused by a number of conditions other than cancer of the ureter or renal pelvis. Symptoms which are severe, get worse, or that last for a few weeks, should always be checked by your doctor.



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How it is diagnosed
Your GP will examine you and organise a series of urine and blood tests. The urine sample will be sent to a laboratory to be checked under a microscope for any cancer cells. Samples of blood will also be taken to check your general health, the number of cells in your blood (blood count), and to see how well your kidneys and liver are working.

Your GP will refer you to a urologist (a doctor who specialises in diseases of the urinary system) if further tests are needed. These tests will help to make the diagnosis and, if cancer is found, to check how far, if at all, the disease has spread.

Cystoscopy and biopsy A small, flexible, fibre-optic telescope (cystoscope) is passed up the urethra to enable the doctor to look at the bladder. The doctor can also extend the tip of the cystoscope up into the ureter: this procedure, known as ureteroscopy, can be done under a local or a general anaesthetic. In most cases it is done under a local anaesthetic because this is the quickest and simplest way.

If any abnormality that could be a cancer is seen, it has to be examined while you are under a general anaesthetic. The doctor will then take a sample of abnormal cells, and these are examined in a laboratory under a microscope by a pathologist (biopsy).

Intravenous urogram or pyelogram (IVU or IVP) This test shows up abnormalities in the urinary system. It is done in the hospital x-ray department and takes about an hour. A dye is injected into a vein, usually in the arm, that travels through the bloodstream to the kidneys. The doctor can watch the passage of dye on an x-ray screen and pick up any abnormalities.

The dye will probably make you feel hot and flushed for a few minutes, but this feeling gradually disappears. You may feel some discomfort in your abdomen, but this will only be temporary. You should be able to go home as soon as the test is over.

Ultrasound scan Sound waves are used to build up a picture of the inside of your body. You may have scans of your bladder and pelvis. The scan will be done in the hospital scanning department. Before your test, you will be asked to drink plenty of fluid so that your bladder is full and a clear picture can be seen. Once you are lying comfortably on your back, a special gel is spread over your abdomen. A small device, like a microphone, is rubbed over the area. The echoes are converted into a picture by a computer. This is a completely painless procedure and takes about 15–20 minutes. Once the scan is over, you will be allowed to empty your bladder.

Retrograde pyelography This is a special x-ray which involves inserting a catheter into the ureter at the time of ureteroscopy. Dye is then passed up the catheter to highlight the ureter and renal pelvis.



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Further tests
If a cancer is found, you may be referred for other tests to find the size of the cancer and whether or not it has spread beyond the ureter or renal pelvis. These may include either of the following:

CT (computerised tomography) scan A CT scan takes a series of x-rays and puts these together to give a 3-D picture of the inside of your body. The scan is painless and takes between 10 and 30 minutes.

You may be asked not to eat or drink anything for several hours before your appointment. Most people who have a CT scan are given a drink or injection of dye before the scan. This helps the doctor to see particular areas more clearly. People who are allergic to iodine or have asthma may be at higher risk of reacting to the dye. If you are allergic to iodine or have asthma, tell the doctor and the person doing the test before you have the injection or drink. After having the injection, most people feel hot and flushed, but this only lasts for a few minutes. You will probably be able to go home as soon as the scan is over.

MRI (magnetic resonance imaging) scan This test is similar to a CT scan, but uses magnetism instead of x-rays to build up cross-sectional pictures of your body. During the test, you will be asked to lie very still on a couch inside a long tube for about 30 minutes. It can be slightly uncomfortable and some people feel claustrophobic during the scan. It is also very noisy, but you will be given earplugs or headphones to wear.

The combination of tests will help the specialist to find out the stage and grade of the cancer. This will help the doctors to decide on the most appropriate treatment for you.



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Staging and grading
Staging
Staging refers to the size of the cancer and whether or not it has spread beyond the ureter or renal pelvis.

The following stages are used for transitional cell cancer of the renal pelvis and ureter:

Localised The cancer is only in the area where it started and has not spread outside the kidney or ureter.
Regional The cancer has spread to the tissue around the kidney or to nearby lymph nodes. Lymph nodes are bean-shaped structures that are found throughout the body. They produce cells that fight infection.
Metastatic The cancer has spread to other parts of the body.
Grading
Grading refers to how abnormal the cancer cells look under the microscope, and can give an idea of whether or not the cancer cells are slow-growing (low-grade) or faster-growing (high-grade).



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Treatment
Treatment will depend on a number of factors, including your age, general health and the position, type, stage and grade of the cancer.

Surgery is the most common treatment for cancer of the ureter and renal pelvis. The extent of surgery will depend on many factors, such as the stage and the grade of the cancer.

After surgery, sometimes further treatment will be recommended, such as radiotherapy or chemotherapy. This is known as adjuvant treatment. The aim of adjuvant treatment is to get rid of any remaining cancer cells and to reduce the chance of the cancer coming back. The effectiveness of adjuvant treatment for cancer of the ureter and renal pelvis is unknown.

If surgery is not possible, other treatments may be more appropriate. These may include chemotherapy or radiotherapy. The aim of these treatments is to reduce the size of the tumour and help control symptoms.

Surgery
Nephro-ureterectomy means the removal of the kidney, ureter and top part of the bladder. Sometimes the surrounding lymph glands, fat and tissue may also be removed.

Segmental ureterectomy resection is the removal of the affected part of the ureter. The remaining parts are then rejoined. This procedure is usually only possible if the tumour is small, low-grade and contained within the ureter.

Ureteroneocystomy (or reimplantation) is the removal of the lower part of the ureter, and sometimes a small part of the bladder. The remaining part of the ureter is then connected to the bladder. This is usually done if the tumour is only in the lower part of the ureter.

Occasionally, a tumour may affect just the surface of the ureter. The cancer may be removed either by laser treatment or electrosurgery. These two surgical treatments are in the early stages of development.

Laser therapy A ureteroscope is passed through the bladder and into the ureter. A narrow beam of intense laser is then passed through the tube to destroy the tumour.
Electrosurgery An electric current is used to remove the cancer. The tumour and surrounding area can be burned away.
Radiotherapy
Radiotherapy treats cancer by using high-energy rays, which destroy the cancer cells and shrink the tumour while doing as little harm as possible to normal cells.

Chemotherapy
Chemotherapy is the use of anti-cancer (cytotoxic) drugs to destroy the cancer cells. They work by disrupting the growth and division of cancer cells. The chemotherapy may be given directly into the vein (intravenously).



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Follow up
After treatment, you will have regular follow-up appointments with your specialist to monitor how you are recovering after treatment. Follow-up will usually include a physical examination. It may also involve taking some urine or blood samples. You will also have regular cystoscopies to detect any changes in the ureter. If you have any problems, or notice any new symptoms between these times, let your doctor know as soon as possible.



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Your feelings
During your diagnosis and treatment of cancer, you are likely to experience a number of different emotions, from shock and disbelief to fear and anger. At times, these emotions can be overwhelming and hard to control. It is quite natural, and important, to be able to express them. Each individual has their own way of coping with difficult situations; some people find it helpful to talk to friends or family, while others prefer to seek help from people outside their situation. Some people prefer to keep their feelings to themselves. There is no right or wrong way to cope, but help is available if you need it.



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Cancer - Renal Pelvis Or Ureter

Definition
The kidneys collect urine in a section called the pelvis. The pelvis and its subdivisions (calyces) empty urine into a tube called the ureter, which leads to the bladder. Cancer can grow in this urine collection system, but is uncommon.

Images:
Kidney anatomyAlternative Names
Transitional cell cancer of the renal pelvis or ureter
Causes, incidence, and risk factors
As a group, renal pelvis and ureter cancers account for no more than 5% of all cancers of the kidney and upper urinary tract. They affect men more often than women and are more common in people older than 65.

Tumors of the renal pelvis and ureter are usually transitional cell cancers. Approximately 10% are squamous cell carcinomas.

The causes of this cancer are not completely known. Chronic (long-term) irritation of the kidney from harmful substances excreted in the urine may be a factor and may result from the following:

•Smoking
•Analgesic nephropathy
•Exposure to aniline dyes and chemicals used in the manufacturing of leather goods, textiles, plastics, and rubber
Patients with a previous history of bladder cancer are also at risk.

Symptoms
•Back pain, located where ribs and spine meet
•Bloody urine
•Burning, pain, or discomfort with urination
•Dark, rust-colored, or brown urine
•Fatigue
•Flank pain
•Need to urinate frequently at night
•Unintentional weight loss
•Urinary frequency or urgency
•Urinary hesitancy
Signs and tests
A physician will examine the abdomen by touch, but it rarely reveals a mass or an enlarged kidney. The patient may have blood in the urine. A complete blood count (CBC) may show anemia.

Cancer cells may appear on the following tests:
•Urine cytology (microscopic examination of cells) obtained during a cystoscopy
•Urine cytology obtained from a urine sample
The tumor, or signs of urinary obstruction, may appear on:
•Intravenous pyelogram (IVP)
•Kidney ultrasound
•Abdominal CT scan
•MRI of abdomen
•Renal scan
An x-ray, CT scan, or MRI of other areas of the body may show that the cancer has spread from the kidneys.
Treatment
The goal of treatment is to eliminate the cancer.

Surgical removal of all or part of the kidney (nephrectomy) is usually recommended. This may include removal of part of the bladder and surrounding tissues or lymph nodes. If the tumor is in the ureter, it may be possible to remove it while preserving the kidney.

When the cancer has spread outside of the kidney or ureter, chemotherapy is often used. Because these tumors behave similarly to transitional cell carcinoma of the bladder, the chemotherapy regimens used are similar to those used for bladder cancer.

Support Groups
For additional information and resources, see cancer support groups.

Expectations (prognosis)
The outcome varies depending on the exact location of the tumor and whether the cancer has metastasized. Cancer localized to the kidney or ureter can be cured with surgery.

Cancer that has metastasized to other organs is usually not curable, though there are exceptions.

Complications
•Local spread of the tumor with increasing pain
•Spread of the cancer
•Kidney failure
Calling your health care provider
Call your health care provider if the symptoms listed above are present.

Prevention
Wear protective equipment if you may be exposed to kidney-poisoning substances. Stop smoking. Follow your health care provider's advice regarding use of medications, including over-the-counter pain medicine

Lung CancerSmoking

Lung cancer is the primary cause of cancer death
In the United States, lung cancer is the primary cause of cancer death among both men and women, killing over 160 thousand people in 2007, which exceeds the combined mortality attributable to breast, prostate and colon cancer. In 2007 there were more than 200 thousand new cases of lung cancer diagnosed in the United States: more among men than women. On average, 1 in 13 men and 1 in 16 women will be diagnosed with lung cancer (a lifetime risk of 8% and 6%, respectively).

Smoking is the single most important risk factor for lung cancer
The single most important factor influencing the risk of developing lung cancer is smoking. In the United States, smoking is estimated to account for 87% of lung cancer cases (90% in men and 85% in women). The lifetime risk of developing lung cancer is 17.2% among male smokers and 11.6% among female smokers. This risk is significantly lower in non-smokers: 1.3% in men and 1.4% in women.

Genetic factors also contribute to risk of developing lung cancer
Epidemiological studies have shown that genetic factors also contribute to the risk of developing lung cancer. Recently, scientists at deCODE Genetics discovered an association between the diagnosis of Lung cancer and two specific variants in the genome. One variant is located on chromosome 15 within the nicotinic acetylcholine receptor gene cluster. In smokers, this same variant also increases the risk for Nicotine Dependence and Peripheral Arterial Disease. The second variant is located on chromosome 5 near the TERT gene.

deCODEme can calculate your genetic risk for lung cancer
The deCODEme Complete Scan and the deCODEme Cancer Scan identify the two risk variants and provide an interpretation of the associated risk for developing lung cancer for individuals of European descent who smoke. More studies need to be conducted to test if the variant also increases risk of lung cancer in people who do not smoke. Currently no risk data are available for people of other ethnicities for these variants.

Risk factors for lung cancer
Smoking is the greatest known risk factor for lung cancer and is estimated to be responsible for approximately 90% of lung cancer in men and 85% in women. Lung cancer risk attributable to tobacco smoking is strongly affected by the duration of smoking, and declines with increasing time from cessation. Thus, the estimated lifetime risk of lung cancer among former smokers ranges from approximately 6% in smokers who give up at the age of 50, to 10% for smokers who give up at age 60, compared to 15% for lifelong smokers and approximately 1% in never-smokers.
Secondary smoke is estimated to cause approximately 3,000 lung cancer deaths per year among non-smokers and contributes to more than 35,000 deaths linked to cardiovascular disease.
Genetics. Regardless of exposure to tobacco smoke, there are important individual differences in the risk of developing lung cancer, some of which are attributable to genetic factors. Thus, for example, even though smoking is the primary cause of lung cancer, only about 15% of lifelong smokers will actually develop this disease. Genetic factors may influence who ends up developing the disease. The role of genetics is further demonstrated by the fact that close relatives of lung cancer patients have an approximately two-fold greater risk of developing the disease compared to the general population.
Environmental pollutants. Exposure to a variety of environmental factors or industrial substances has been associated with increased risk of lung cancer. These include asbestos, radon and arsenic. Certain lung diseases can also increase the risk for lung cancer. However, these factors combined still contribute much less to the disease risk than tobacco smoking.
The best way to prevent lung cancer is not to smoke
The best way to avoid lung cancer by far is not to smoke and to avoid second-hand smoke and other environmental factors that may increase the risk of the disease.

Dietary choices may affect lung cancer
There is some evidence that suggests that a diet rich in fruit may have protective effect against lung cancer. Furthermore, smokers may benefit from eating vegetables. Several large studies have been conducted in order to test if intake of vitamins or other supplements might protect against lung cancer. To date, there is limited evidence that this might be the case. Highly publicized studies of beta-carotene and vitamin A supplementation in smokers actually showed an increase in lung cancers in the supplementation groups. In another study of over 75,000 individuals it was shown that the long-term use of supplemental multivitamins, such as vitamin C, vitamin E, and folate did not reduce the risk of lung cancer. On the contrary, the results of the study indicated that high doses of vitamin E might even increase the risk of lung cancer.

Lung cancer screening
Individuals who are identified as being at high risk for lung cancer may be referred to have chest X-rays or sputum cytology examination. In addition, a spiral CT scan is a newly-developed procedure for lung cancer screening. Numerous lung cancer screening trials are currently taking place but presently, the U.S. Preventive Services Task Force (USPSTF) concludes that evidence is insufficient to recommend for or against screening asymptomatic persons for lung cancer.

Treatment options for lung cancer
The outcome of lung cancer depends on the tumor type, how advanced the disease is when it is diagnosed, and the general health of the person diagnosed. Overall, lung cancer is one of the most difficult cancers to treat. If the disease is diagnosed early, then more treatment options are available and prognosis is better. Treatment options include surgery, radiation, chemotherapy, or a combination of these

Lung Cancer - Smoking Related Facts

It is well documented that cigarette smoke is the major cause of lung cancer (primary carcinoma of the lung) and is a cause of chronic lung disease. As well as lung cancer, tobacco smoke contributes to cancer of the bladder, pancreas, and kidney.

It is actually the chemicals and compounds in tobacco smoke that make smoking so harmful. Read more about the harmful effects of smoking.

•Primary carcinoma of the lung is the leading cause of cancer deaths in both men and women.
•It accounts for approximately 32% of cancer deaths in men and 25% in women.
•Current or former cigarette smokers make up approximately 90% of patients with lung cancer.
•Men who smoke one pack a day increase their risk 10 times compared with non-smokers.
•Men who smoke two packs a day increase their risk more than 25 times compared with non-smokers
•Of the 180,000 people diagnosed in the United States alone each year, 86% will die within 5 years of diagnosis.
What Is Lung Cancer?
There are two major types of lung cancer:

•Non-small cell lung cancer - consists of 3 types:
◦Squamous cell carcinoma
◦Ademocarcinoma and
◦Large cell carcinoma
•Small cell lung cancer also called oat cell cancer. It usually spreads to different parts of the body more quickly than non-small cell and accounts for about 20% of all lung cancer
Causes Of Lung Cancer
Smoking is the number one cause of lung cancer. The more you smoke and the longer you smoke, the greater your risk.

If you stop smoking however, the risk of lung cancer decreases. Year on year, abnormal cells are replaced by normal cells. After ten years, the risk drops to a level that is one-third to one-half of the risk for people who continue to smoke.

There are also many more benefits.

•Quitting smoking greatly reduces the risk of developing other smoking-related diseases, such as heart disease, stroke, emphysema and chronic bronchitis.
Lung cancer normally takes many years to develop. Incidence tends to peaks between the ages of 55 and 65 years. The changes in the lung however can begin almost as soon as a person is exposed to carcinogenic chemicals.

Soon after exposure begins, a few abnormal cells may appear in the lining of the bronchi (the main breathing tubes). Gradually as you continue your exposure to these substances, more abnormal cells appear. Some will become cancerous and tumour forming.

Primary Lung Cancer Secondary Lung Cancer - Mesothelioma

Cancer is a disease related to the uncontrolled growth of tissue, leading to the accumulation of mass (called a tumor or lesion.) Normal cells in the body divide and grow in an orderly controlled manner. When cells grow uncontrollably and this growth invades other tissues or organs, the growths are called malignant or cancerous. When a mass of tissue, or tumor, is benign, it is relatively stable and does not invade other tissues.

Cells from malignant tumors can break away and travel to other parts of the body, usually through the bloodstream, but also through the lymph system. When these cells find new host organs, these cells can grow into tumors in the new tissue. This spreading process is called metastasis and when a cancer has reached an advanced stage to where the malignant cells are attacking other organs, it is said that the cancer tumors have metastasized. The tumors in new organs are always made up of cells similar to those of the original tumor.

Benign tumors do not metastasize. They can often times be removed through surgery and not re-occur.

Lung Cancer
Lung cancer occurs when lung tissue develops cancerous growths. Primary lung cancer is cancer that originates in the lung tissue. Secondary lung cancer is cancer that spreads, or metastasizes, from other organs.

Primary Lung Cancer
There are several different types of primary lung cancer. These are divided into two main groups:

•Small Cell Lung Cancer
•Non-small Cell Lung Cancer
Pleural mesothelioma is often thought of as a third type of primary lung cancer. However, it is not a lung cancer. Mesothelioma does not develop in the lungs, but in the serous membranes surrounding the lungs. As such, it does not fall into the typical categories of lung cancer. Mesothelioma can also occur in other tissues, in the lining of the abdomen, call peritoneal mesothelioma, and in the lining of the heart, pericardial mesothelioma.

Small Cell Lung Cancer
Small Cell Lung Cancer comprises approximately 20% of the primary types of lung cancer. It is called small cell cancer because the tumor cells are very small, with the cells containing almost exclusively the cell nucleus and nothing more. This type of cancer is also referred to as �oat cell� cancer. Chemotherapy is often suggested for this cancer in the early stages because of the rapid way it which it spreads. Surgery is not a good option to stop the spread early on. This type of cancer is most closely linked to smoking; non smokers rarely have it.

Non-Small Cell Cancer
Non-small cell cancer falls into these categories:

•Squamous cell carcinoma
•Adenocarcinoma
•Large cell carcinoma
•Adenosquamous cell carcinoma
•Undifferentiated carcinoma
Each category of non-small cell cancer are physiologically similar and they respond to treatment differently than to small cell lung cancer.

Squamous cell carcinoma is a common type of primary lung cancer. This type of cancer is also linked to smoking and it develops from the cells than line the airways in the lungs. Squamous cells are thin, flat cells that look like fish scales. Commonly the tumor growths are located in the center of the lungs near the large airways (bronchi). It is also referred to as epidermoid carcinoma. It comprises approximately 30 to 35% of the non-small cell cancer in the US, affecting men and the elderly most frequently.

Adenocarcinoma, like squamous cell carcinoma, develops from tissues in the lung airways. But, it develops from the glandular secretory tissues. (tissues that produce mucus). It is often found in the outer airway passages, not the main bronchi, like the squamous cell variety. The incidence of this cancer is increasing. It comprises about 40% of the non-small cell lung cancer in the US and is the most common lung cancer among women.

Large cell lung cancer is named after its appearance. The cells look large and unnatural under the microscope. These types of cells grow quite quickly.

Adenosquamous carcinoma are cells that appear flat under the microscope, like the squamous cells, but derive from the glandular secretory cells, like the adenocarcinoma.

Undifferentiated carcinoma includes cancer cells that cannot be identified as one of the other groups. The cells appear abnormal under the microscope and multiply uncontrollably.

Secondary Lung Cancer
Secondary lung cancer is cancer that has spread to the lungs from other organs. Many different types of cancer spread to the lungs, because of its very high blood supply. These include breast cancer and colon cancer.

The type of cancer is very important when it comes to treatment. The different types of cancer cells respond differently to different types of chemotherapy and other therapies. When cancer cells spread from other organs to the lungs, then the lungs have to be treated for the other type of cancer, not lung cancer. This is an important distinction. For example, breast cancer that spreads to the lungs, has to be treated for breast cancer, not lung cancer.

Pancreatic Cancer

The pancreas is a gland behind your stomach and in front of your spine. It produces juices that help break down food and hormones that help control blood sugar levels. Cancer of the pancreas is the fourth-leading cause of cancer death in the U.S. Some risk factors for developing pancreatic cancer include

Smoking
Long-term diabetes
Chronic pancreatitis
Certain hereditary disorders
Pancreatic cancer is hard to catch early. It doesn't cause symptoms right away. When you do get symptoms, they are often vague or you may not notice them. They include yellowing of the skin and eyes, pain in the abdomen and back, weight loss and fatigue. Also, because the pancreas is hidden behind other organs, health care providers cannot see or feel the tumors during routine exams. Because it is often found late and it spreads quickly, pancreatic cancer can be hard to treat. Possible treatments include surgery, radiation and chemotherapy.

Prostate Cancer

What is the prostate gland?

The prostate gland is an organ that is located at the base or outlet (neck) of the urinary bladder. (See the diagram.) The gland surrounds the first part of the urethra. The urethra is the passage through which urine drains from the bladder to exit from the penis. One function of the prostate gland is to help control urination by pressing directly against the part of the urethra that it surrounds. Another function of the prostate gland is to produce some of the substances that are found in normal semen, such as minerals and sugar. Semen is the fluid that transports the sperm. A man can manage quite well, however, without his prostate gland. (See the section on surgical treatment for prostate cancer.)

In a young man, the normal prostate gland is the size of a walnut. During normal aging, however, the gland usually grows larger. This enlargement with aging is called benign prostatic hypertrophy (BPH), but this condition is not associated with prostate cancer. Both BPH and prostate cancer, however, can cause similar problems in older men. For example, an enlarged prostate gland can squeeze or impinge on the outlet of the bladder or the urethra, leading to difficulty with urination. The resulting symptoms commonly include slowing of the urinary stream and urinating more frequently, particularly at night.

What is prostate cancer?

Prostate cancer is a malignant (cancerous) tumor (growth) that consists of cells from the prostate gland. The tumor usually grows slowly and remains confined to the gland for many years. During this time, the tumor produces little or no symptoms or outward signs (abnormalities on physical examination). As the cancer advances, however, it can spread beyond the prostate into the surrounding tissues (local spread). Moreover, the cancer also can metastasize (spread even farther) throughout other areas of the body, such as the bones, lungs, and liver. Symptoms and signs, therefore, are more often associated with advanced prostate cancer.

Why is prostate cancer important?

Prostate cancer is the most common malignancy in American men and the second leading cause of deaths from cancer, after lung cancer. Most experts in this field, therefore, recommend that beginning at age 40, all men should undergo yearly screening for prostate cancer.

Kidney Cancer

The kidneys

The kidneys are a pair of organs on either side of the spine in the lower abdomen. Each kidney is about the size of a fist. Attached to the top of each kidney is an adrenal gland. A mass of fatty tissue and an outer layer of fibrous tissue (Gerota's fascia) enclose the kidneys and adrenal glands.

The kidneys are part of the urinary tract. They make urine by removing wastes and extra water from the blood. Urine collects in a hollow space (renal pelvis) in the middle of each kidney. It passes from the renal pelvis into the bladder through a tube called a ureter. Urine leaves the body through another tube (the urethra).

The kidneys also make substances that help control blood pressure and the production of red blood cells.


Understanding cancer

Cancer begins in cells, the building blocks that make up 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.
◦Usually, benign tumors can be removed, and they seldom grow back.
◦Cells from benign tumors do not invade tissues around them or 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 they can grow back.
◦Cells from malignant tumors can invade and damage nearby tissues and organs. Also, cancer cells can break away from a malignant tumor and enter the bloodstream or lymphatic system. That is how cancer cells spread from the original cancer (primary tumor) to form new tumors in other organs. The spread of cancer is called metastasis.
Several types of cancer can start in the kidney. This booklet is about renal cell cancer, the most common type of kidney cancer in adults. This type is sometimes called renal adenocarcinoma or hypernephroma. Another type of cancer, transitional cell carcinoma, affects the renal pelvis. It is similar to bladder cancer and is often treated like bladder cancer. Wilms tumor is the most common type of childhood kidney cancer. It is different from adult kidney cancer and requires different treatment. Information about transitional cell carcinoma and Wilms tumor is available from the Cancer Information Service at 1-800-4-CANCER and at http://cancer.gov.

When kidney cancer spreads outside the kidney, cancer cells are often found in nearby lymph nodes. Kidney cancer also may spread to the lungs, bones, or liver. And it may spread from one kidney to the other.

When cancer spreads (metastasizes) from its original place to 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 kidney cancer spreads to the lungs, the cancer cells in the lungs are actually kidney cancer cells. The disease is metastatic kidney cancer, not lung cancer. It is treated as kidney cancer, not lung cancer. Doctors sometimes call the new tumor metastatic or "distant" disease.

Cancer in Pregnancy

Pregnancy should not delay treatment of cancer. Treatment is similar to that in nonpregnant women except for rectal and gynecologic cancers.

Because embryonic tissues grow rapidly and have a high DNA turnover rate, they resemble cancer tissues and are thus very vulnerable to antineoplastic drugs. Many antimetabolites and alkylating drugs (eg, busulfan Some Trade Names
MYLERAN
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, chlorambucil Some Trade Names
LEUKERAN
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, cyclophosphamide Some Trade Names
CYTOXAN
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, 6- mercaptopurine Some Trade Names
PURINETHOL
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, methotrexate Some Trade Names
RHEUMATREX
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) can cause fetal abnormalities. Methotrexate Some Trade Names
RHEUMATREX
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is particularly problematic; use during the 1st trimester increases risk of spontaneous abortion and, if the pregnancy continues, multiple congenital malformations. Although pregnancy often concludes successfully despite cancer treatment, risk of fetal injury due to treatment leads some women to choose abortion.

Rectal cancer: Rectal cancers may require hysterectomy to ensure complete tumor removal. Cesarean delivery may be done as early as 28 wk, followed by hysterectomy so that the infant can be saved and aggressive cancer treatment started.

Cervical cancer: Pregnancy does not appear to worsen cervical cancer. Cervical cancer can develop during pregnancy, and an abnormal Papanicolaou (Pap) test should not be attributed to pregnancy. Abnormal Pap tests are followed by colposcopy and directed biopsies when indicated. Usually, conization can be avoided. If biopsy shows mild dysplasia, normal delivery is possible, and follow-up evaluation can start 6 wk postpartum. Severe dysplasia or carcinoma in situ warrants further evaluation during pregnancy; colposcopy is usually accurate, but sometimes biopsy is necessary.

For carcinoma in situ (Federation of Gynecology and Obstetrics [FIGO] stage 0—see Table 7: Gynecologic Tumors: Clinical Staging of Cervical Carcinoma*) and microinvasive cancer (stage IA1), treatment is often deferred until after delivery because conservative options may be possible then.

If invasive cancer (FIGO stage IA2 and higher) is diagnosed during early pregnancy, immediate therapy appropriate for the cancer is traditionally recommended. If invasive cancer is diagnosed after 20 wk and if the woman accepts the unquantified increase in risk, treatment can be deferred until into the 3rd trimester (eg, 32 wk) to maximize fetal maturity without prolonged delay until cancer treatment. When hysterectomy is delayed until delivery, some experts recommend that it be done immediately after delivery. Others recommend delaying hysterectomy until 6 wk postpartum because risks due to hysterectomy are thought to be much greater at delivery due to the increased blood supply to the pelvic organs at that time.

In certain cancers, chemotherapy may induce tumor regression, allowing the fetus to mature to a viable stage before definitive treatment (surgery or radiation therapy). Delivery is usually cesarean, but vaginal delivery, although controversial, may be as safe.

Other gynecologic cancers: After 12 wk gestation, ovarian cancer is easily missed; then, the ovaries, with the uterus, rise out of the pelvis and are no longer easily palpable. If very advanced, ovarian cancer during pregnancy may be fatal before completion of the pregnancy. Affected women require bilateral oophorectomy as soon as possible. Endometrial and fallopian tube cancers rarely occur during pregnancy.

Leukemia and Hodgkin lymphoma: These disorders (see Leukemias; see Lymphomas) are uncommon during pregnancy. Antineoplastic drugs typically used increase risk of fetal loss and congenital malformations. Because leukemias can become fatal rapidly, treatment is given as soon as possible, without any significant delay to allow the fetus to mature. If Hodgkin lymphoma is confined to above the diaphragm, radiation therapy may be used; the abdomen must be shielded. If lymphoma is below the diaphragm, abortion may be recommended.

Breast cancer: Breast engorgement during pregnancy may make recognizing breast cancer difficult. Any solid or cystic breast mass should be evaluated.

Overview of Colon Cancer Symptoms

It's best to get regular screenings rather than rely on colon cancer symptoms to alert you to the presence of a tumor. This is because colon cancer can grow for years before causing any symptoms. But, knowing what to look out for can't hurt.

Constipation
Constipation, having a bowel movement less than three times a week, can be your body's way of suggesting that you make some minor adjustments in diet or exercise. However, constipation can also be a symptom of a colon cancer. In the beginning of the colon, waste material is slushy and can easily maneuver around anything that gets in its way. But as it nears the end of the colon, stool solidifies and is less forgiving of obstacles. A tumor in the rectum or far end of the colon can make it very difficult for waste to get by, thereby causing constipation.

Thin Stool
Once stool is no longer in its slushy phase and begins to take shape, how it looks when it leaves your body can provide clues to what's going on inside. For example, thin stool can sometimes indicate that your waste squeezed by some sort of obstacle on its way out. In the case of colon or rectal cancer, that obstacle would be a tumor in the latter part of the colon or the rectum.

Stomach Cramps
Sometimes a tumor causes a bowel obstruction, which is basically a road block in your colon. Depending on the severity of the blockage, solids, liquids, and even gas may be prevented from passing by. This leads to abdominal cramps that can be severe, especially if the blockage restricts blood flow to the colon. Painful cramps may also indicate that a tumor has perforated (poked through) the bowel wall; bowel perforation is a medical emergency.

Hematochezia (Bloody Stool)
Tumors tend to bleed -- not a whole lot and not constantly, but they do bleed. As a result, some of that blood may show up in your stool. If the tumor is in the beginning of the colon, the blood will most likely be dry and virtually invisible by the time the waste leaves your body. However, if the tumor is in the rectum or toward the end of the colon, it may still be fresh and therefore, bright red.

Unexplained Weight Loss
Many of us wouldn't want to question unexplained weight loss. We'd just be happy to be losing weight! But unfortunately, effortless weight loss is generally a sign that something is wrong. In the case of colon cancer, unexplained weight loss can be a sign that a tumor is releasing chemicals that are increasing your metabolism.

Sense of Fullness
A tumor that grows toward the end of the colon or in the rectum may cause a sense of fullness. This is because your body senses that there's something else hanging around by its exit. What it doesn't know is that it's a tumor and it's attached, so it isn't going anywhere. It basically sees the tumor as a stubborn piece of waste, so you get that "I still have to go" sensation that can't be relieved.

Nausea and Vomiting
Nausea and vomiting can occur for a lot of reasons. Motion sickness, an unpleasant sight or smell, a slew of common viruses, and drinking too much are all familiar causes. But sometimes, nausea and vomiting can be symptoms of something more serious, such as colon cancer.

Gas and Bloating
A pattern of gas and bloating may be an indication that a tumor is growing in the colon and occasionally causing a blockage. Even if the tumor isn't large enough to cause a bowel obstruction on its own, stool may periodically get hung up on the tumor while it's passing by, causing a temporary obstruction. While your bowel is blocked and air is trapped, you'll be bloated. When the blockage resolves itself, all that air will need somewhere to go and you'll be gassy.

Lethargy
Sometimes the presence of a tumor causes iron deficiency anemia, a condition that can cause you to feel extremely tired (lethargic). Tumors tend to bleed, which results in a loss of iron -- an element that transports oxygen to your cells. This symptom is characteristic of tumors in the beginning of the colon. Since it's pretty roomy there, tumors can get fairly big and bleed a lot before causing any other colon cancer symptoms. The blood usually dries before leaving the body, too, which also allows the bleeding to go unnoticed.

The Bottom Line
Even though you have an idea of what to look out for, it's important to remember that a tumor can grow for years before causing any colon cancer symptoms. In addition, all of these symptoms are very poor predictors in and of themselves.

For most people, the best way to prevent colon cancer is to maintain a healthy lifestyle and receive regular screenings starting at age 50.

Section of Cancer Genetics

Section Highlights
The major scientific focus of the Section of Cancer Genetics is the study of inherited susceptibility to cancer. Most common types of human cancer include a proportion of cases that are attributable to inherited susceptibility to the disease. Individuals carrying susceptibility genes are frequently at very high risk of developing cancer that is often diagnosed at an early age. Study of this group of people is important for two major reasons:

•Identification of individuals who are at high risk before they develop the disease may allow them to take avoiding action
•Elucidation of the genetic mechanisms underlying the susceptibility often generates important insights into the development of the common forms of non-familial cancer
Within the last few years the availability of new technologies to investigate the whole genome in substantial numbers of cases has allowed expansion of our research to investigation of genetic variants with smaller increases in cancer risk, at a population level. Although the risks associated with such genetic variants are much smaller, they are often present in many people and can therefore be making an appreciable contribution to cancer. Major advances in the discovery of this class of predisposition gene are anticipated over the next few years.

The Section of Cancer Genetics includes research programmes studying predisposition to a wide range of adult cancers, including breast cancer, colorectal cancer, prostate cancer, testis cancer, thyroid cancer and leukaemia. In addition, we have one of the few research programmes investigating predisposition to childhood cancers. These programmes range from mapping and identifying the genes responsible, through characterisation and evaluation of their importance, to the implementation of the findings in the clinic.

The Cancer Genome Project was established by Professor Mike Stratton and Dr Richard Wooster at the Wellcome Trust Sanger Institute at Hinxton. The availability of the finished human genome sequence provided the platform from which the systematic search for somatically acquired abnormalities in DNA of cancer cells could be launched. The close collaboration between the Wellcome Trust Sanger Institute and The Institute enables both Institutions to maximise their contributions to a major medical research aim of the next decade: the exploitation of the human genome sequence in cancer research.



Recent Highlights

Breast Cancer: In 2006 we reported three breast cancer predisposition genes, ATM, BRIP1 and PALB2. Mutations in these genes are rare in the UK population and double the risk of breast cancer. The genes all act in pathways that repair damaged DNA and interact with the known breast cancer genes BRCA1 or BRCA2.

Childhood Cancer: In 2006 we also showed that very rare individuals with two (biallelic) mutations in PALB2 develop a serious childhood development disorder known as Fanconi anemia and have a very high risk of childhood cancer. Biallelic mutations in two other breast cancer genes, BRCA2 and BRIP1, have also been shown to lead to subtypes of Fanconi anaemia.

Prostate Cancer: 2006 saw the start of a large, unique international study of targeted screening for prostate cancer in men with an increased risk of the disease – the IMPACT study.

Colorectal Cancer: In 2006 we reported a new susceptibility locus for colorectal cancer on chromosome 3q21. We also reported the results of a large-scale genome-wide association study of nonsynonymous single nucleotide polymorphisms which suggests that variants in the GH-IGF and DNA damage response pathways may influence disease risk.

Progress in Childhood Cancer

Since the mid-1950s, cooperative research has improved the survival rates for childhood cancer from less than 10% to almost 80% overall. Cure rates vary according to each specific type of childhood cancer. Some types remain very difficult to cure. All cure rates need to be improved.

Multi-institution cooperative research of major scope has also paid dividends well beyond childhood cancer, contributing to:

•understanding the abnormal biology of cancer cells,
•treatments for adults with cancer,
•developing principles of team management for other diseases of children and adults, and
•pioneering the enormous advantages of multi-institution cooperation in clinical research.
Important Steps in the History of Childhood Cancer Research

Multi-institution Cooperation in Clinical Trials
One of the most important contributions to developing better treatments for children with cancer was the formation by the National Cancer Institute of the first group of hospitals that agreed to cooperate in clinical trials of new drugs that had been developed to treat acute leukemia, the most common cancer among children.

Cooperative clinical trials of chemotherapy for acute leukemia were begun at seven hospitals scattered through the U.S. in 1955. Research grant support was provided by the NCI.

Leukemia Chemotherapy
The original seven member hospitals of the group were convened by the National Cancer Institute to cooperate in conducting trials of new chemotherapy for acute leukemia. This was the optimal way to quickly evaluate new chemotherapies that showed promise in laboratory experiments on leukemia cells. The first cancer clinical trials cooperative group treated only one type of childhood cancer; acute leukemia, using only one modality of treatment: chemotherapy. The era of chemotherapy for cancer had been heralded by discovery of several chemical agents that could eliminate leukemia cells from the bone marrow and circulating blood in children with acute leukemia. This was a breakthrough that demanded rapid trials of many potentially effective new agents. The NCI developed groups of institutions to cooperate in joint conduct of clinical trials to perfect new chemotherapies being developed in many laboratories. National cooperation in clinical research was very successful. Many new agents were found to be effective in treating acute leukemia and gradually the remissions of leukemia extended from several months to several years. At that time, however, there was little discussion of cures.

Treatment of Solid Tumors in Children
Due to the success of chemotherapy in acute leukemia, it was imperative to try chemotherapy against the cancers of solid organs. The NCI supported childhood cooperative research group pediatric surgeons, pediatric radiation oncologists and pediatric pathologists to their membership, in order to combine surgery, chemotherapy and radiation therapy in treating the solid malignant tumors of children. After a few years, the group required multi-disciplinary teams to be formed at each member institution. The group which had been formed originally to test chemotherapy for leukemia, was significantly re-organized to include the principal medical disciplines needed to diagnose and treat solid tumors of children as well as leukemia.

Multi-Disciplinary Team Care of Childhood Cancer
Childhood cancer groups developed special national studies combining surgery, chemotherapy and radiation therapy to treat certain types of cancers of the kidneys and muscles which occurred mainly in children. Combined modalities of treatment, including surgery, chemotherapy and radiation therapy were found to produce the best results for these childhood solid tumors after surgical removal of as much of the tumor as possible.

New treatments based on immunology, bone marrow and stem cell transplantation and newer treatments derived from molecular biology and genetics are now in increasingly wider use as the research horizon expands. Multi-institution clinical trials by cancer clinical researchers are the most efficient way to apply new laboratory discoveries to advance diagnosis, selection of the most appropriate treatment and, increasingly, to prevent cancer.

The best response and survival rates of children with cancer have been achieved by treatment according to a clinical trial protocol at a cooperative group member hospital with experience in conducting multi-disciplinary clinical trials. To participate in cooperative national clinical trials, a member institution now must have a multi-disciplinary team of experts that can comply with all diagnosis, treatment, supportive care and laboratory requirements of cooperative clinical trial protocols and provide combinations of treatments adjusted to the needs of each child.

Laboratory and Translational Research on Childhood Cancer
Research in cellular and molecular biology, genetics, immunology and epidemiology has become an important aspect of cooperative group cancer research. To improve diagnostic evaluation, to develop new treatments and to evaluate how they affect cancer cells, many group member institutions developed laboratory research programs to further accelerate progress in diagnosis, treatment and cure of all types of cancers that attack children. The cooperative groups have incorporated laboratory research programs in many basic sciences. These have led to new understandings of how normal cells transform into cancer cells and how to develop therapies to overcome that process without harm to normal cells and tissues. Current treatments that directly affect only cancer cells are referred to as “targeted” therapy. Many of the important discoveries of the Human Genome Project have led to better diagnosis and treatments.

The majority of the laboratory researchers conducting research related to childhood cancer are located at academic medical centers throughout the U.S. and Canada. When they produce laboratory research findings which have potential application to diagnosis, treatment, supportive care or prevention of childhood cancer, they have ready access to their clinical colleagues on the COG team at their institution. One of the primary objectives of the COG is to facilitate the translation of important laboratory research to clinical applications to benefit children with cancer. This has been a research priority of COG institutions for several decades.

The Concept of Total Cure
A major emphasis for the past two dozen years has been on improving the quality of life for patients cured of cancer during childhood. The modern definition of “cure” for children goes far beyond achieving disappearance of the evidences of cancer. It now includes the goals of psychosocial, educational, and occupational reintegration of the child into a successful life. In social terms, the impact of this achievement is considerable: The cure of a child saves an entire lifetime.

The Genetics of Cancer

The ancient Greeks believed that cancer was caused by too much body fluid they called "black bile." Doctors in the seventeenth and eighteenth centuries suggested that parasites caused cancer. Today, doctors understand more about the link between cancer and genetics. Viruses, ultraviolet (UV) radiation, and chemicals can all damage genes in the human body. If particular genes are affected, a person can develop cancer.

Genes and chromosomes

Genes are the basic functional and physical unit of heredity that is passed on from parent to child. They are made of deoxyribonucleic acid (DNA) and are located on structures called chromosomes in every cell of a person's body. Genes direct much of what happens in the body, such as the determination of eye color, blood type, and in some cases, the development of cancer.

The human body contains nearly 30,000 genes, which are located on 46 chromosomes (arranged in 23 pairs) in every cell of a person's body. Genes come in pairs, and a person inherits one gene in each pair from the mother and the other from the father. Chromosome pairs 1 through 22 are numbered chronologically (in order) and are called autosomes. The remaining two chromosomes (the 23rd pair) are the sex chromosomes and determine whether someone is born female or male.

How genes cause cancer

For various reasons, genes often undergo mutations (changes). Some mutations have no effect on a cell, while other mutations are harmful or helpful to the cell. There are two basic kinds of genetic mutations. If the mutation is passed from one of the parents to the child, it is called a germline mutation. When a germline mutation is passed on from a parent to the child, it is present in every cell of the child's body, including the reproductive sperm and egg cells. Because the mutation affects reproductive cells, it is passed from generation to generation. Germline mutations are responsible for 5% to 10% of cancer cases. This is also called familial (occurring in families) cancer.

Most cancers are caused by a series of mutations that develop during a person's lifetime called acquired mutations. Acquired mutations are caused by tobacco, over-exposure to UV radiation, and other toxins and chemicals. These mutations are not in every cell of the body and are not passed from parent to child. Cancer caused by this type of mutation is called sporadic cancer.

Most scientists believe that cancer happens when several genes of a particular group of cells become mutated. Some people may have more inherited mutations than others, and even with the same amount of environmental exposure, some people are simply more likely to develop cancer.

Genes that play a role in cancer

The following types of genes contribute to cancer:

Tumor suppressor genes. These are protective genes. Normally, they suppress (limit) cell growth by monitoring the rate at which cells divide, repairing mismatched DNA, and controlling cell death. When a tumor suppressor gene is mutated (due to heredity or environmental factors), cells continue to grow and can eventually form a tumor. Close to 30 tumor suppressor genes have already been identified, including BRCA1, BRCA2, and p53. In fact, nearly 50% of all cancers involve a missing or damaged p53 gene.

Oncogenes. These genes turn a healthy cell into a cancerous one. HER2/neu and ras are two common oncogenes.

DNA repair genes. These are genes that fix any mistakes made when DNA is replicated (copied). Mistakes that aren't fixed become mutations, which may eventually lead to cancer, especially if the mutation occurs in a tumor suppressor gene or oncogene.

Cancer develops when several genes in a cell become mutated in a way that overrides the checks and balances of the cell. However, many cancers cannot be tied to a specific gene, and some genes may interact in unpredictable ways with other genes or factors in the environment to cause cancer. In the future, doctors hope to learn more about the role of genetic changes in the development of cancer, which may lead to improved cancer treatment and prevention strategies.

Genetic factors - Childhood cancer

A small proportion of childhood cancer cases (less than 5%) have an obvious family history.

The most important example of a childhood cancer for which there are familial aggregations of cases is retinoblastoma; about 40% of the cases of this tumour are heritable.

Such aggregations also occur, though to a much smaller extent, for Wilms' tumour. The pattern of inheritance for the heritable form of retinoblastoma is relatively simple and is well understood; that for Wilms' tumour is more complicated.

In addition, certain childhood cancers are associated with rare inherited conditions such as neurofibromatosis, tuberous sclerosis, Fanconi's anaemia, ataxia telangiectasia, and xeroderma pigmentosum, though the actual number of cases of childhood cancer in which these conditions occur is small. In these and other rare conditions more than one child, and also other family members, may have an associated cancer.

Familial aggregations, involving both child and adult cases, also occur in the 'Li-Fraumeni syndrome' which is associated with mutations in the TP53 gene.

There are also associations with various chromosome abnormalities; the most important of these is Down syndrome which occurs in a small percentage of cases of childhood leukaemia: the risk of acute leukaemia among children with Down syndrome is between 10 and 30 times as high as that for other children.1

The striking ethnic distribution of Ewing's sarcoma, which is almost absent from black populations both in Africa and the USA, suggests that genetic influences are important in the aetiology of this tumour.

It is clear from these and other observations that the causes of some childhood cancers are partly genetic. For a detailed discussion of genetic factors in the epidemiology of childhood cancers.2

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Retinoblastoma
There are about 45 cases of retinoblastoma in Great Britain each year, and about 20 of these are of the type that can be inherited. The pattern of inheritance is that of an autosomal dominant condition with a high degree of penetrance, though the disease is actually the result of mutation in the tumour suppressor gene RB1.

Retinoblastoma may be either bilateral, that is, affecting both eyes, or unilateral. All bilateral cases are heritable; a few unilateral cases are known to be heritable because a related family member also has retinoblastoma. Nearly half the children of a parent with heritable retinoblastoma will themselves be affected.

For children of cases not known to be heritable the estimated risk is very low, around 1%. Likewise if there is no previous family history the risks for siblings of unilateral and bilateral cases are respectively about 1% and 2%.3

Using modern molecular genetics and pre-natal screening more definite advice about the risk can often be obtained.

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Risk to siblings
When a child is diagnosed with cancer it is likely that questions will be raised concerning the risks to the siblings of the affected child. Sometimes a second sibling will be affected by cancer purely as a result of chance; in other cases such an occurrence may reflect an increased risk in particular families.

In the general population the chance of a child developing cancer is about 1 in 500. In the absence of a relevant clinically observed genetic condition in the child, or a family history of such a disease, or a 'cancer syndrome', and excluding twins, the risks for siblings of affected children are about double what would be expected by chance, giving a risk of 1 in 250; this is the risk that such siblings will develop cancer between birth and age 15.4

It should be emphasised that the risk is less than 1 in 250 for siblings who are already part way through childhood when the affected child is diagnosed, and have therefore passed part of the period when they would be at risk.

The risks are considerably higher if the affected child is a member of a family affected by one of the genetic conditions referred to above. The existence of such a condition may actually be recognised as a result of a second sibling being affected. In fact, many familial aggregations of childhood cancer can, sometimes retrospectively, be recognised as forming part of a known genetic condition or syndrome.5

But, for genetic counselling, risk estimates sometimes have to be made before such knowledge becomes available for a particular family, and in this situation the estimated doubling of the population risk for the siblings of affected cases is appropriate.

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Risk to twins
For a child with cancer who has a twin the situation is different. For dizygotic (nonidentical) twins of affected children, although there is little direct evidence, it can be assumed that the risks are the same as they would be for other siblings in the same family.

For monozygous (identical) twins there is a high risk for the co-twins of children with leukaemia, especially those diagnosed in the first year of life.6 In this case the risk for co-twins appears to be usually, if not always, attributable to the transfer of leukaemic cells from one twin to the other during pregnancy.

An identical twin of a child with retinoblastoma also has a high risk of developing retinoblastoma, though the actual level of risk will vary a great deal, depending on whether or not there is a family history and whether the tumour is bilateral or unilateral.

For other childhood cancers there is insufficient information to make any estimate of risk, but it seems likely that identical co-twins of affected children will have a high risk of developing the same disease.

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Risk for offspring of children with cancer in the absence of known genetic disease in the family
Now that large numbers of children survive their cancer and go on to have children of their own, there is inevitably concern about whether their offspring will have an increased risk of cancer.

In general, after the exclusion of hereditary cancer syndromes, there is no evidence of a significantly raised risk of cancer among the offspring of survivors.7

The Genetics of Prostate Cancer

What are genes?

Genes are small individual collections of information within each cell of the human body. Each gene is made of a unique sequence of DNA. Researchers working on the Human Genome Project have estimated that there are as many as 30,000 different genes in each cell. Genes are packaged onto chromosomes. There are 23 pairs of chromosomes in each cell. One chromosome of each pair is inherited from the person's father and one from the person's mother.

Genes control how a cell functions, including how quickly it grows, how often it divides, and how long it lives. To control these functions, genes produce proteins that perform specific tasks and act as messengers for the cell. Therefore, it is essential that each gene have the correct instructions or "code" for making its protein so that the protein can perform the proper function for the cell.

What role do genes play in prostate cancer?

Cancer begins when one or more genes in a cell are mutated (changed), creating an abnormal protein or no protein at all. The information provided by an abnormal protein is different from that of a normal protein, which can cause cells to multiply uncontrollably and become cancerous.

A person may either be born with a genetic mutation in all of their cells (germline mutation) or acquire a genetic mutation in a single cell during his or her lifetime. An acquired mutation is passed on to all cells that develop from that single cell (called a somatic mutation). Most prostate cancer (about 75%) is considered sporadic, meaning that the damage to the genes occurs by chance after a person is born. Familial (runs in the family) prostate cancer is less common (about 20%) and occurs because of a combination of shared genes and shared environmental or lifestyle factors. Hereditary (inherited) prostate cancer is rare (about 5%) and occurs when gene mutations are passed within a family, from one generation to the next.

What are the chances a mutated gene is inherited?

Every cell usually has two copies of each gene: one inherited from a person’s mother and one inherited from a person’s father. Hereditary prostate cancer appears to follow an autosomal dominant inheritance pattern, in which a mutation needs to happen in only one copy of the gene for the person to have an increased risk of getting the disease. This means that a parent with a gene mutation may pass on a copy of the normal gene or a copy of the gene with a mutation. Therefore, a child who has a parent with a mutation has a 50% chance of inheriting that mutation. A brother, sister, or parent of a person who has a gene mutation also has a 50% chance of having the same mutation.

What is a man's average risk for prostate cancer?

A man with an average risk for prostate cancer has about a 14% chance of developing prostate cancer by age 80. The risk of prostate cancer is slightly higher for black men than for white men.

How common is prostate cancer?

Prostate cancer is the most common cancer and the second most common cause of cancer death for men. In 2009, an estimated 192,280 men in the United States will be diagnosed with prostate cancer. It is estimated that 27,360 deaths from this disease will occur this year. Although the number of deaths from prostate cancer is declining among all men, the death rate remains more than twice as high for black men than for white men.

How can a man know if he has inherited a genetic mutation that increases his risk of prostate cancer?

Only genetic testing can determine whether a man has a genetic mutation, but there are no genetic tests available to specifically determine a man's chance of developing prostate cancer. Currently, there is not one gene that definitively causes prostate cancer, although some genes or gene mutations have been shown to be more common for men with prostate cancer. Research to identify genes associated with an increased risk of prostate cancer is ongoing, and men with a strong family history of prostate cancer may be eligible to participate in such studies.

For more information, read about Genetic Testing and Clinical Trials.

How does a man know if prostate cancer runs in his family?

A man may have an increased risk of developing prostate cancer if two or more close relatives have prostate cancer. Familial prostate cancer is when two or more first-degree relatives (father, brother, son) are diagnosed with prostate cancer. Hereditary prostate cancer is when a family has any of the following characteristics:

Three or more first-degree relatives with prostate cancer
or

Prostate cancer in three generations on the same side of the family
or

Two or more close relatives (father, brother, son, grandfather, uncle, nephew) on the same side of the family diagnosed with prostate cancer younger than age 55
Not all doctors agree with the same definitions for familial prostate cancer and hereditary prostate cancer, but the terms are used to help researchers and doctors learn more about these groups of patients and their family histories. Having a family history of prostate cancer does not necessarily mean that a man will develop prostate cancer.

What is a man's risk if prostate cancer runs in his family?

If a man has a first-degree relative with prostate cancer, his risk of developing prostate cancer is two to three times greater than the average risk. The risk increases as more relatives are diagnosed with prostate cancer. Researchers have made progress in understanding how certain changes in the DNA of cancer cells can cause normal prostate cells to become cancerous, and this information may help doctors understand how prostate cancer can run in families.

Most experts strongly recommend that people concerned about a family history of prostate cancer first consult a genetic counselor. Genetic counselors are trained to determine the possibility of hereditary cancer risk for a family and can identify appropriate genetic testing or research studies.

Which inherited genetic mutations raise the risk of prostate cancer?

Researchers continue to find genes that may be associated with an increased risk of prostate cancer. However, more research is needed to better understand these genes before genetic testing can be used to determine a man’s risk of developing prostate cancer.

One gene known to increase the risk of prostate cancer, by as much as three times the average risk, is located on chromosome 17. The normal function of this gene is not known, but men who inherit a mutated version of the gene have a 44% higher level of the prostate-specific antigen (PSA) protein, a protein in the blood used to help diagnose prostate cancer. However, not everyone with this gene will develop prostate cancer.

Other genes that may cause an increased risk of developing prostate cancer, include HPC1, HPC2, HPCX, and CAPB. Research on these genes is still new and genetic tests are not yet available for routine screening because it is not clear that they definitely cause prostate cancer.

Are there other genetic conditions associated with an increased risk of prostate cancer?

Men with BRCA1 and BRCA2 (BRCA stands for BReast CAncer) gene mutations have an increased risk of prostate cancer. BRCA1 and BRCA2 gene mutations are most commonly associated with hereditary breast and ovarian cancer (HBOC) syndrome. Men with BRCA1 mutations have a slightly increased risk, while men with BRCA2 mutations have about a 20% risk of developing prostate cancer during their life, usually before age 65. For this reason, men with BRCA1 or BRCA2 gene mutations are encouraged to begin annual prostate cancer screening at age 40. Men with BRCA1 or BRCA2 gene mutations also have an increased risk of breast cancer.

BRCA1 and BRCA2 are tumor suppressor genes. A tumor suppressor gene makes proteins that prevent tumor formation by limiting cell growth. Mutations in a tumor suppressor gene causes a loss of the ability to restrict tumor growth and, as a result, cancer can develop. Genetic testing for the BRCA1 and BRCA2 genes is available. However, mutations in BRCA1 and BRCA2 are thought to be responsible for only a small percentage of familial prostate cancer cases. Genetic testing may only be appropriate for families with prostate cancer that may also have HBOC.

For more information, read the Cancer.Net Guide to Hereditary Breast and Ovarian Cancer.

What is a man's risk level?

In addition to family history, other environmental and lifestyle factors may influence the risk of prostate cancer. Discussing family history and personal risk factors with a doctor can help a man better understand his risk. If a man has a higher than average risk, he may consider genetic counseling and early detection screening.

A risk factor is anything that increases a person's risk of developing cancer. Having a particular genetic mutation linked to prostate cancer cannot predict that a man will develop cancer. Controllable risk factors, such as eating a balanced, heart-healthy diet (a diet low in saturated fat, cholesterol, and sodium), maintaining a healthy weight, exercising, limiting alcoholic beverages, and avoiding tobacco products also play a role. Research to better understand the link between genetic mutations and prostate cancer is ongoing. Talk with a doctor for more information about risk factors, prevention, and screening for prostate cancer

How Do Abnormal Genes Cause Cancer?

In their normal form, BRCA1 and BRCA2 genes prevent breast cancer by producing a protein that stops cells from growing out of control. Every person (women and men alike) has two copies of each of these genes in most cells in her or his body.

As long as at least one gene in each pair is working properly, breast cells function normally. But if both copies of a breast gene are abnormal, they no longer can stop abnormal growth. In this case, breast cells multiply much more than normal. And some can invade healthy tissue. The result is what we call invasive breast cancer. (In non-invasive breast cancer, cells grow too much but haven't started to invade normal surrounding healthy tissue.)

All breast cancers are caused by abnormal genes. The abnormalities, or mutations, in the genes can be either inherited or acquired:

Inherited genetic abnormality: Some people are born with an abnormal gene passed on by a parent. They have one abnormal gene from that parent and one normal gene from the other parent.
Acquired (or non-hereditary) genetic abnormality: A gene can became abnormal as a result of wear and tear, through an error in how the gene reproduces, or from a variety of other factors — toxic exposure, environmental effects, diet, hormonal influences, or unknown causes. Acquired genetic abnormalities account for 85% to 90% of breast cancers.
Whether you inherited an abnormal breast cancer gene or acquired it, if you have one normal gene, that gene will still work to control cell growth and prevent cancer. But if that normal gene breaks down, for whatever reason, then cancer results