How cancer starts
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Doctors and scientists now know that each cancer starts with changes in one cell or a small group of cells. Usually, many years before you can feel a lump, or a doctor can see it on a scan, the cells have started to divide and reproduce uncontrollably.
You can see from the differences between normal cells and cancer cells that the cancer cell seems to lose a number of vital control systems. This happens because some of the genes in the cell have been damaged or lost. Scientists call this 'mutation'.
Genes are coded messages inside a cell that tell it how to behave. Different genes tell the cell how to make different proteins. One gene codes for one protein. Each cell has many genes and can therefore make many different proteins.
Proteins are the building blocks that make up a cell. Some proteins act as on and off switches that help to control how a cell behaves. For example, a hormone signal acts on a protein in or on the cell. The protein then sends a series of signals which tell the cell to reproduce by dividing into two.
Mutation means that a gene has been damaged or lost. A mutation may mean that too much protein is made. Or that a protein is not made at all.
For example, a signaling protein may be permanently switched on. Or other proteins, whose job is to control and limit cell division, may be permanently switched off.
Something that damages a cell and makes it more likely to be cancerous is called a carcinogen. For example, there are carcinogens in cigarette smoke. There is more about this in the section about causes and cancer.
Some genes encourage cells to multiply or double. Normally, in adults, this would not happen very often. Cells would only multiply to repair damage, for example after a wound or operation. But if these genes become abnormal, they tell the cell to multiply all the time. Scientists call these genes oncogenes. This really means cancer genes.
Some genes are in the cell specifically to stop the cell multiplying or doubling. If one of these 'tumour suppressor genes' becomes damaged and stops working, then the cell may carry on and on multiplying. In other words it becomes immortal, which is one of the properties of a cancer cell. The best known tumour suppressor gene is called p53. This gene normally stops cells with other damaged genes from reproducing and encourages them to destroy themselves (apoptosis). p53 is damaged or missing in most human cancers.
These genes normally repair any damage to the DNA that makes up the cell's genes. If these DNA repair genes are damaged, then other mutations are not repaired and the cell can copy the mutations when it divides and multiplies. These genes have been found to be damaged in some human cancers, including bowel cancer.
Mutations can happen by chance when a cell is reproducing. It is not easy for a normal cell to turn into a cancer cell. There have to be about half a dozen different mutations before this happens. Cells often destroy themselves if they have a mutation. Or the immune system might recognise them as abnormal and kill them. This means most precancerous cells die before they can cause cancer. Only a small number of the changes turn into a cancer. There is detailed information in our section about the immune system.
It can take a long time before enough mutations happen for a cell to become cancerous. This is why most types of cancer are more common in older people. There has been more time to be exposed to carcinogens. And more time for accidents to occur when cells reproduce.
Some people are said to have a genetic predisposition to a type of cancer. This means they are more likely to develop that type of cancer than most other people. They are more at risk of cancer because they have been born with one of the mutations that starts to make a cell cancerous. They do not actually have the cancer because more than one mutation is needed for a cancer to develop. There are many steps in the process of a normal cell becoming a cancer cell. But people with particular mutations are naturally further along the road towards getting certain types of cancer than people who don't have the mutation.
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