New insight into the role of the breast cancer gene known as BRCA2

Researchers at the Medical Research Council (MRC) Cancer Cell Unit, Cambridge have gained an important new insight into the role of the breast cancer gene known as BRCA2.

It appears to have a key function in cell division which needs to happen accurately for normal cell reproduction and repair, otherwise disease occurs. The findings are published today (29 Friday October 2004) in the journal Science.

Around 30 to 50 per cent of breast cancers that run in families are thought to occur because the BRCA2 gene is not working. People who inherit defective BRCA2 are not only more susceptible to breast cancer, but also have a higher risk of developing cancers of the ovary, pancreas and prostate.

The researchers found that where there was a mutation in the BRCA2 gene, cells failed to divide accurately and acquired an incorrect number of chromosomes.*

The final critical step where cells divide is called cytokinesis. This is where a cell separates into two to create replicas of itself known as ‘daughter cells’. It is at this point that a full set of chromosomes is put together for each of the new cells. Any malfunction in this process can result in cells having too few or too many chromosomes or abnormalities, which have implications for disease.

Since the discovery of the breast cancer susceptibility genes BRCA1 and BRCA2, researchers have sought to identify exactly why mutations in these genes lead to breast cancer. Understanding the role BRCA2 has in cell division and chromosome separation sheds light on this mechanism and what happens when it goes wrong.

The research team which includes Medical Research Council and Cancer Research UK (CR-UK) scientists was led by Professor Ashok Venkitaraman, Deputy Director of MRC Cancer Cell Unit and member of the University of Cambridge CR-UK Department of Oncology.

Professor Venkitaraman said: “Our research shows that BRCA2 works to link cell division with proper chromosome separation. Cancer cells frequently gain or lose chromosomes, but how this happened was not known until now.

“We already know that cancer cells with highly abnormal numbers of chromosomes often respond poorly to therapy so it is important to understand how this comes about. In future it may be possible to use the results of our study to come up solutions that form the basis of effective new treatments for this type of tumour.

Matthew Daniels, one of the research team added: “It is possible that similar problems occur in non-hereditary cancers. A greater understanding of these processes will help us work towards prevention and better management of cancers.”

The research was funded by the MRC, CR-UK and an AstraZeneca studentship to Cambridge University Clinical School.

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