Month: March 2019

Gene linked to prostate cancer

Researchers have discovered a gene that appears to be associated with prostate cancer and how fast it grows. Overactivity of this gene appears to cause cells to divide uncontrollably – resulting in cancer. It is hoped that a test for this gene’s activity could be developed that could be used to identify prostate cancer and distinguish between slow-growing and fast-growing tumours.

The work was conducted by researchers at the Institute of Cancer Research Everyman centre and have been published in the journal Oncogene (Foster CS, Falconer A, Dodson AR. Transcription factor E2F3 overexpressed in prostate cancer independently predicts clinical outcome. Oncogene advance online publication, 7 June 2004).

What is prostate cancer?

The prostate is the gland that produces the liquid component of semen. It is only found in men and is located just below the bladder. Cancer of the prostate gland cause tumours to develop in the prostate, which becomes enlarged.

How many people are affected by prostate cancer each year?

According to Cancer Research UK, more than 27,000 men are diagnosed with prostate cancer every year.

According to the NHS Cancer Screening programmes, approximately 10,000 men die from the disease every year. This means that many men develop prostate cancer but do not die from it – in fact, only 1 in 25 men will die from the disease. This is because many forms of prostate cancer are slow-growing and the men can live out their lives without suffering any ill effects from the tumour.

What is the risk of developing prostate cancer?

The overall lifetime risk of developing prostate cancer for a man is one in 14. In other words 73 in every 1,000 men will develop prostate cancer in the whole of their lifetime.

However, age plays in important role: prostate cancer is largely a disease of older men. Men aged less than 50 years rarely develop prostate cancer, while half of all cases of prostate cancer are in men aged more than 75 years.

How is prostate cancer detected?

If it is suspected that there is a problem with your prostate, the following tests may be carried out.

Urine test – to look for blood in the urine or to see if the problems are due to an infection.

PSA blood test – a blood sample is tested for its level of prostate-specific antigen (PSA), a high level may suggest prostate cancer, however it may also be due to a less harmful cause.

Digital rectal examination – a urologist feels the prostate by inserting his or her finger into the back passage. The urologist can then feel for any abnormalities that may suggest prostate cancer.

However, none of these tests can confirm that a person has prostate cancer. For example, some men may have prostate cancer, but their PSA levels are normal. Meanwhile, two out of every three men who do have a raised PSA level do not have prostate cancer. Instead, their raised levels are due to either infection, exercise, sex or benign enlargement of the prostate (often known as BPH or benign prostatic hypertrophy).

The only way to confirm the presence of prostate cancer is to remove a section of the prostate and study it under the microscope – known as a biopsy. Even then it cannot be accurately known whether or not the cancer is slow-growing (and does not need treating) or is fast-growing (and should be treated).

For this reason, researchers are looking for a test that will accurately diagnose prostate cancer and show whether or not it is slow- or fast-growing.

What did the researchers find?

A gene, known as E2F3, plays an important role controlling cell division and growth. Overactivity of the E2F3 gene is thought to result in uncontrolled cell division and growth, leading to the development of a tumour. For this reason, the researchers decided to investigate whether or not E2F3 played a role in the development of prostate cancer.

The researchers found high levels of E2F3 activity in 98 out of 147 samples of prostate cancer (67 per cent). High levels of E2F3 activity are rarely found in samples of normal prostate tissue.

In addition, the researchers found that there was a significant association between high levels of E2F3 activity and the risk of death from prostate cancer. This suggests that increasing levels of E2F3 activity are associated with increasingly fast-growing cancers (also known as aggressive cancers).

Why is this important?

The findings suggest that it might be possible to develop a test for E2F3 activity that could help to diagnose whether or not a person has prostate cancer with greater accuracy than is currently possible.

Also, the findings suggest that such a test would be able to show whether or not the cancer was fast- or slow-growing.

Why is it important to find out how fast a prostate cancer is growing?

Because prostate cancer occurs in later life, many men with slow-growing prostate cancer can live out their natural lives without suffering any ill effects. They don’t need treatment. However, the aggressive form will shorten a man’s life and needs to be treated as soon as possible.

By being able to distinguish between the types of prostate cancer, many men will be spared treatment they did not need.

When will a test be available?

The researchers’ work is currently in the very early phases of development and it could be many years before a working test for the activity of E2F3 becomes available.

Aspirin associated with lower breast cancer risk

Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) have been found to be associated with a reduced risk of developing breast cancer. In a study published in the Journal of the American Medical Association (JAMA) women who regularly took aspirin for pain relief were found to have a 20 percent lower risk than women who did not take the painkiller. Aspirin is also thought to help protect against other cancers, for example of the bowel and colon.

However, the current recommendations are that women should not start to take aspirin to help prevent breast cancer because the painkiller is associated with other, unwanted, side-effects such as gastrointestinal problems.

Below we look at the issue in more depth:

By how much did aspirin and NSAIDs reduce the risk of developing breast cancer?

Women who had taken aspirin at least once a week for six months had a 20 percent lower risk of developing breast cancer.

Women who took at least seven aspirin tablets a week (the equivalent of at least one a day) had their risk of breast cancer reduced by 28 per cent.

Women who took NSAIDs also reduced their risk of developing breast cancer, but the effect was not as great as it was for aspirin.

Women who took painkillers that were not aspirin or NSAIDs did not have a reduced risk of developing breast cancer.

Should women take aspirin regularly to reduce their risk of breast cancer?

No. The benefits of taking aspirin and NSAIDs regularly need to be balanced against the risks of long-term use: for example long-term aspirin use has been found to cause stomach ulcers and bleeding of the stomach lining. For this reason, until more research has been carried out, aspirin and NSAIDs cannot be recommended as a long-term preventive treatment for breast cancer.

Does aspirin help to protect against all forms of breast cancer?

No. Aspirin and NSAIDs appear to only help to protect against breast cancers that are stimulated by oestrogen. These “hormone receptor-positive” cancers are the most common form of breast cancer.

However, because of the way that aspirin and NSAIDs work, they have no effect on hormone receptor-negative cancers.

Why is it that aspirin only has an effect on hormone receptor-positive cancers?

Hormone receptor-positive breast cancers are affected by the levels of oestrogen and progesterone present in breast tissue. The higher the levels of these hormones, the more the cancer cells are stimulated to grow and divide. Aspirin and NSAIDs help to reduce the risk of hormone receptor-positive breast cancer by reducing the levels of oestrogen.

Aspirin and NSAIDs reduce the amount of oestrogen in breast tissue by acting on a mechanism that controls oestrogen production. The final step in the production of oestrogen is controlled by a catalyst called aromatase cytochrome P450 and the amount of catalyst is controlled by prostaglandins. While the amount of prostaglandins is controlled by an enzyme called cyclooxygenase (COX) and this enzyme is affected by aspirin and NSAIDs. Aspirin and NSAIDs prevent COX from making prostaglandins, which in turn reduces the amount of aromatase produced, which in turn reduces the amount of oestrogen produced.

How was the study carried out?

The study was carried out by researchers at the University of Columbia who looked looked at 1442 women with breast cancer and 1420 women without breast cancer. The women were asked about their use of aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) and non-NSAID painkiller paracetamol. The results of the study were published in the 26 May 2004 issue of the Journal of the American Medical Association (JAMA 2004: 291; 2433-2440).