Publications
Partners
The findings could help doctors spot those patients who stand to benefit most from particular treatments, and also give insights into how medicines lose their effectiveness.
Reporting in the journal Nature, researchers at the Institute of Cancer Research in the United Kingdom, noted that healthy BRCA2 is actually a tumour suppressor. But a defective form of the gene renders cells incapable of fixing damaged DNA, which in turn encourages malignancy.
The new research was conducted with both breast and ovarian cancer cells. The research team found that after exposure to standard chemotherapy, some cells mutate back to the normal BRCA2 gene type. This allows the cells to overcome DNA damage, but it does not neutralise the tumour. It does, however, neutralise the effectiveness of the cancer drugs, leading to drug resistance.
"The research deepens our understanding of why some breast cancer patients with a faulty BRCA2 gene may stop responding to treatment," Prof Herbie Newell, executive director of translational research at Cancer Research UK, told the BBC. "This type of research is becoming increasingly important as we seek to tailor cancer therapies to individual patients," he said.
Read more:
Cancer Centre
February 2008
