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New Discovery may Help Develop Drugs That Kill Cancer Cells

by VR Sreeraman on  December 27, 2009 at 7:37 AM Cancer News   - G J E 4
 New Discovery may Help Develop Drugs That Kill Cancer Cells
Scientists claim to have identified a family of "limpet-like" proteins that appears to play a vital role in repairing DNA damage which triggers cancer.
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They hope that the finding may lead to new drugs, which could help kill cancer cells, and promote production of healthy replacements.

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The Small Ubiquitin-like Modifier (SUMO) proteins appear to have a remarkable ability to zero in on the damaged areas.

They bind to normal proteins and direct them in to repair genetic glitches.

With this method, the proteins were even able to repair double strand DNA breaks - the most severe type of DNA damage.

And after the work is complete, the proteins detach themselves and move on.

The researchers focussed their study on BRCA1 gene, which, if damaged, is associated with a very high risk of breast cancer.

SUMO was shown to attach to the damaged gene, and switch it back on - helping prevent breast cancer forming.

"This new insight is the first step towards developing drugs which may protect normal cells from the side effects of chemotherapy, or improve the effectiveness of current breast cancer treatments," BBC News quoted Researcher Dr Jo Morris, from King's College London, as saying.

"DNA damage, particularly double strand DNA breaks, are a fundamental cause of cancer and we know that people who have mutations in the BRCA1 gene have a higher risk of developing some kinds of cancer," said Dr Lesley Walker, of Cancer Research UK, which part-funded the study

"Discovering that these limpet-like proteins play such an important role in repair may provide new opportunities to stop cancer from growing.

"This is an extremely complex and intricate biological process so it may be many years before we can use this knowledge to safely intervene and help treat cancer patients," she added.

The study appears in journal Nature.

Source: ANI
SRM
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