HEALTH / Second Opinion

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The Independent Culture
IF ASKED the cause of cancer, many people would say it is still unknown. But in fact our understanding of the causes of the disease has expanded substantially over the past 20 years. By identifying a cancer gene called P53, researchers feel they have made a very big advance. Already, large numbers of external factors have been identified. These include cigarette smoking, alcohol and excess exposure to sunlight, as well as less well known triggers such as the hepatitis B virus and the Epstein-Barr virus (the cause of glandular fever in Western countries but of a cancer of the lymph glands in tropical Africa). Other less common but important causes include chemicals such as asbestos and aromatic amines, and nuclear radiation.

But why should there be genes that predispose people to cancer? This is the third aspect of cancer that is becoming more clearly understood as a result of research into cell growth. With a few exceptions, such as brain neurones, the cells that make up most parts of the body continue to divide and grow throughout life - a slow process. Some, however, such as those in the lining of the intestine, are replaced within 18-24 hours. Damaged skin and other tissues are quickly replaced, but healthy structures grow only as large as they need to be and no larger.

The capacity of cells to grow and multiply has to be controlled very efficiently if it is not to run out of control, and evolution has developed an elaborate system to do this. The control of cell growth is a function of a group of genes; in cancer the growth-controlling genes become defective. Around 100 or so of the 100,000 human genes are classed as oncogenes - genes that may become defective and then may lead to a cancer developing. Current thinking is that several genes in one cell need to become defective to disturb growth sufficiently for a cancer to develop. Malfunction of one or two genes may be enough to produce a harmless tumour such as a wart or a breast cyst, but if more of the brakes on growth are removed then the tumour may escape from all control and become a life-threatening, invasive cancer.

Researchers have now identified several of the genes that most often malfunction. The most common is a gene known as P53, which is found to be defective in about half of all human cancers. P53 is a tumour-suppressor gene, the normal function of which is to halt unhealthy multiplication of cells. It is easily damaged, however, and among the external cancer triggers that are known to damage it are ultraviolet radiation in sunlight and the aflatoxin mould that grows on peanuts and maize and is an important cause of liver cancer in tropical Africa. Some people inherit a partly defective P53 gene, but in most cases it is external factors that do the damage. If several other oncogenes have also been damaged then the scene is set for a cancer to start growing.

For the first time, cancer researchers are getting close to the biological mechanisms that switch a cancer on. Already the identification of genes such as P53 in a cancer give guidance on its likely response to treatment. The ultimate hope is that it should eventually be possible to find ways to turn the cancer switches off without doing any harm to other parts of the body.

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