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Inheritence of Faulty Tumor Supressor Gene may Lead to Breast Cancer

by Jayashree on  August 31, 2007 at 11:23 AM Cancer News   - G J E 4
Inheritence of Faulty Tumor Supressor Gene may Lead to Breast Cancer
Scientists in London and Italy have identified a tumour suppressor gene, which can raise the risk of breast cancer even if one copy of it is faulty.

Women typically inherit a copy of the Tip60 gene each from their mothers and fathers, say the researchers.
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Normally, tumour suppressor genes lose their function if both their copies are faulty, but Tip 60 can have its activity reduced even if one of its copy is faulty, say the researchers.

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While studying biopsies, the researchers discovered that low Tip60 activity was particularly associated with aggressive tumours.

The scientists also found that low activity of Tip60 was associated with the development of breast cancer because the gene did not work as actively in breast cancer tissue as it did in normal tissue.

The new findings had implications for the treatment of women afflicted by breast cancer, said the scientists.

"More aggressive types of breast cancers tend to recur after treatment, spread to other parts of the body, and respond less well to chemotherapy," the BBC quoted said Dr Tim Crook, the team leader at The Breakthrough Breast Cancer Research Centre, as telling Nature magazine.

"The identification of Tip60's role in breast cancer is a step forward towards predicting the aggressiveness of the disease and then individualising chemotherapy for women," Dr. Crook added.

According to Antonia Dean of Breast Cancer Care, scientists are still a long way from fully understanding the role genes play in the development of breast cancer, "and how this interacts with or is mediated by other factors".

"This is initial research. Further studies are needed to fully determine how these findings can be translated into practical benefits for people with breast cancer and the exact role Tip60 may have in the development of the disease," Dean said.

Source: ANI
JAY/S
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