London, February 11 : Scientists have discovered that mechanism by which found out breast and ovarian cancers caused by a faulty BRAC2 gene may develop resistance to treatment.
The researchers say that the faulty BRAC2 gene renders cells unable to repair damaged DNA, which can lead to them becoming cancerous.
They say that drugs like PARP inhibitors and carboplatin, the platinum-based chemotherapy drug, have been shown to be particularly effective against BRAC2 tumours in early laboratory trials.
Such therapies work by causing yet more DNA damage, tipping the cancer cells over the edge and killing them off, they add.
However, while more advanced trials of the drugs are currently underway in patients with BRAC2 breast and ovarian cancer, there are concerns that some tumours would develop resistance.
The researchers say that it has been observed in the latest phase of the research on tumour cells that after exposure to the drugs, some cells are able to mutate back to the normal BRAC2 gene, allowing them to overcome DNA damage.
However, this might potentially neutralise the impact of the drugs, instead of neutralising the tumour, they say.
According to them, the same effect has been found in tumour tissue taken from women with ovarian cancer.
Professor Alan Ashworth, director of the Breakthrough Breast Cancer Research Centre, says considers this finding to be a clear example of Charles Darwin's natural selection theory, suggesting that cancer cells are able to survive by changing the way treatments affect them.
"Drug resistance is a problem common to all types of cancer, yet this important process is poorly understood. Our work has shown how this occurs in some women with cancer. In the future we hope to be able to use this information to predict whether cancer patients will benefit from particular treatments," the BBC quoted him as telling Nature magazine.
"By understanding this process, we can alter patient treatment to counter the problem of resistance," he added.
Professor Herbie Newell, Cancer Research UK's executive director of translational research, said: "This research deepens our understanding of why some breast cancer patients with a faulty BRCA2 gene may stop responding to treatment.
"This type of research is becoming increasingly important as we seek to tailor cancer therapies to individual patients," Professor Newell added.