How a cancer gets its blood supply
This page tells you about how a cancer gets its blood supply. There is information about
A cancerous tumour is made up of billions of cancer cells. The tumour gets bigger because the number of cells increases. Each individual cell goes through a growth cycle again and again, doubling into two cells each time. There is more about this in our section about cells and cancer.
As the tumour gets bigger, the centre of it gets further and further away from the blood vessels in the area where it is growing. So the centre of the tumour gets less and less of the oxygen and the other nutrients all cells need to survive.
In fact, scientists researching how tumours grow think that a cancer can't grow much bigger than a pin head before it needs to develop its own blood supply. Until it grows its own blood supply, the tumour cannot grow any bigger because the cells at the edge of the tumour will die due to lack of oxygen. There is information lower down this page about how cancers develop their own blood supply.
Cancer at this very early stage is often called 'carcinoma in situ'. This just means that it is very small and hasn't spread into the surrounding area, or spread anywhere else in the body. Some researchers think that cancers get to this point and may stop developing for many months or years.
These cancers are still so small that they will probably not be found unless they are somewhere where they are easy to spot, for example in the skin, or on the cervix (where they can be found during a smear test). A carcinoma in situ in an internal organ will usually be too small to pick up on a scan. The exceptions are breast cancer and cervical cancer. Carcinomas in situ can be picked up on mammograms and in cervical smears.
Normal cells can stimulate new blood vessels to grow. This happens to repair damaged tissue when wounds are healing and is called 'angiogenesis'. So, normal cells have genes that can produce proteins called angiogenic factors, which switch blood vessel growth on. Cells also have genes that produce proteins called antiangiogenic factors, which switch blood vessel growth off.
Researchers into angiogenesis think that this is the big difference between a carcinoma in situ and a growing cancer. They think that for some time, a carcinoma in situ may not be able to spread - it is 'dormant'. Then, it may suddenly begin to be able to trigger tiny blood vessels called capillaries to grow. The cancer can then begin to grow again and spread into the body tissues around it.
The tumour cells may have mutated and lost antiangiogenic genes (the 'off switches' for blood vessel growth). Or their angiogenic genes ('on switches') may have become permanently switched on. It is possible that both these things have happened and it is the balance between the two that is important. The tumour cells may also be able to stimulate other normal cells to produce angiogenic factors.
Once a tumour can stimulate the growth of blood vessels, it can grow bigger and grow more quickly. It will stimulate the growth of hundreds of new capillaries from the nearby blood vessels to bring it nutrients and oxygen.
Scientists also think angiogenesis may play a part in cancer spread. They have found that the newly developing capillary cells release substances that help the cancer cells to detach from the primary tumour and get into the bloodstream. This means that the cells can travel to another part of the body and begin to grow there.
Angiogenesis may also explain why a secondary cancer can appear years after the primary. Sometimes, cancer cells that have spread may not yet be able to stimulate the growth of blood vessels. A small secondary could develop, similar to a carcinoma in situ. The cells continue to multiply and mutate, but the cancer cannot get much bigger.
Through mutation, the cells may suddenly begin to be able to trigger blood vessel growth many months or even years later. A secondary cancer would then begin to grow rapidly and would grow large enough to cause symptoms or show up on a scan.
A lot of research is going on into angiogenesis. The research has found that the amount of these angiogenic factors is very high at the outer edges of a tumour. Anti-angiogenic drugs may stop a cancer from growing into surrounding tissue or spreading. They will probably not be able to get rid of a cancer, but may be able to shrink it or stop it growing in some cases. Researchers have already found some anti-angiogenic drugs that can control some types of cancer. More of these drugs are being developed and tested all the time. You can find out about trials into anti-angiogenic drugs on our clinical trials database. Examples of drugs that interfere with blood vessel growth are
Anti-angiogenic factors do not affect normal blood vessels, only newly growing ones. There is detailed information about anti-angiogenesis treatment in the section about biological therapies.
Doctors are also using this research to look at predicting how a cancer will behave. Some cancers have higher concentrations of tumour blood vessels than others in their outer edges. Doctors think that it may be these cancers that are more likely to spread. If doctors can predict that a cancer is not likely to spread, then patients can be spared the more intensive treatment that some others may need.
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