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Immune-Boosting Drugs Could Enhance Cancer Treatment

Dec. 14, 2009 — Stimulating the body's own immune system to fight cancer offers new treatment opportunities for cancer patients, and scientists have made the first step towards finding existing drugs that could help.


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In findings recently published in the British Journal of Cancer, a study by scientists at St George's, University of London shows that two existing cancer drugs have the ability to stimulate the body's immune cells (white blood cells) into attacking invading cancer cells. This could improve patient survival and recovery by expanding treatment options and lessening the side effects that are often caused by current cancer treatment. But the researchers warn that there is much more research to be done before patients will benefit.

"The reason the body's own immune system doesn't kill cancerous cells is because they camouflage themselves as healthy cells. This means our white blood cells aren't able to recognise the cancerous cells as being a problem. As a result, cancer is able to continue to spread, undetected by the immune system," explains lead researcher Dr Wai Liu.

Current cancer-fighting drugs help cure patients by killing cells directly, stunting their growth, or starving them to death by cutting off their nutrition. In practice, patients will be often prescribed a treatment that combines the drugs' effects, so treatment is likely to include an element of cell killing.

The drugs that cure the illness by killing cancerous cells directly -- known as cytotoxics -- work by targeting the area of the body affected by the disease and killing as many cells as possible within that area. The down side to this is that, although cancerous cells are killed, the drugs are non-discriminatory so will also attack the body's healthy cells, including those responsible for boosting the immune and recovery systems.

With funding from the Cancer Vaccine Institute, specialist cancer researchers at St George's, Dr Liu and Professor Angus Dalgleish, investigated how effective three existing cytotoxic cancer-fighting drugs -- cyclophosphamide, oxaliplatin (ox) and gemcitabine (gem) -- were at stimulating the immune system into fighting cancer cells. They found that both ox and gem were effective, whilst cyclophosphamide did not stimulate the immune cells.

In lab based experiments conducted with human cells outside the body, the researchers showed that these drugs stimulate the immune system in three stages. They begin by hijacking the tumour and forcing it to switch off its camouflage so it becomes visible to the body's immune system. The tumour is then forced to throw out a signal to the body's defence system, which highlights its presence and encourages white blood cells to attack the now visible cancer cells. The white blood cells responsible for communicating that there is an invasion are also boosted and quickly spread the news that there is a problem to those cells responsible for killing 'foreign' cells.

"Cancer treatment is continually being fine-tuned to help us find more and better ways of eradicating the disease. Using the body's own immune system is a relatively new way of thinking in the development of cancer treatments. If successful, it could potentially see patients taking less medication, having fewer and less severe side effects and recovering quicker. And because the treatment enhances the body's natural defences which are present all around the body, it could potentially be effective in treating all types of cancers," says Dr Liu.

The next stage of the research will be to test the drugs' effectiveness in animals and, if this mirrors the success of the lab based results, the researchers will begin tests in patients.

"These findings strengthen hope for a new ways of improving cancer treatment," says Dr Liu. "But, this research is only the first stage of investigations and so far has analysed the reaction of human blood outside body, so much more work is needed before these findings can be used in practice," he concludes.

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The above story is reprinted from materials provided by University of St George's London.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


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