Dr Feng Tang Yang from the Department of Clinical Veterinary Medicine, University of Cambridge, and scientists at the Babraham Institute have discovered that a tiny change in a protein involved in cell survival is responsible for abnormal cell activity in the early stages of cancer.

The discovery, described in an article in Cancer Cell published on 19 January 2004, was made by Dr Rui Zhao, working in Dr Denis Alexander's research group at the Babraham Institute, Cambridge. Dr Zhao noticed that the tiny change in Bcl-xL that normally occurs after exposing cells to radiation no longer happened when the particular cancer gene was present.

The protein, known as Bcl-xL, normally protects cells from dying. When the DNA in cells becomes damaged, Bcl-xL is modified so that it no longer keeps the cells alive. In the presence of a particular cancer gene, the usual modification of Bcl-xL following DNA damage doesn't occur, so cells with DNA damage are kept alive, resulting in cancer.

Intriguingly, the cancer gene being studied at the Babraham Institute (a hyperactive tyrosine kinase) acts by a 'double-whammy' mechanism. In the first instance, it inhibits the rapid repair of DNA damage that often occurs as cells divide. Therefore DNA damage quickly begins to accumulate in cells containing the cancer gene. Additionally, the cancer gene prevents the cells with damaged DNA from being eliminated, so leading to cancer.

Understanding how the cancer gets going in the first place might eventually lead to novel cancer therapies. Dr. Alexander's group has also shown that the critical modification of Bcl-xL, prevented by the cancer gene even before the cancer gets started, also remains blocked in tumours even when they've been exposed to reagents used in chemotherapy.

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