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Study supports DNA repair-blocker research in cancer therapy
Date:8/17/2009

he repair process?

The investigators showed that a key player in DNA repair -- the BRCA1 protein best known in its mutated form as an inherited breast cancer risk factor -- couldn't fulfill its mission in lung cancer cells lacking cdk1.

Going a step further, the researchers administered a cdk-inhibiting drug to lung cancer cells that hadn't been stripped of their cdk1 protein. In these cells, BRCA1 activity was reduced, demonstrating that the cdk inhibitors work in large part by keeping BRCA1 on the sidelines, weakening the DNA repair team.

"These results explain the observations seen in clinical trials" currently being conducted at Dana-Farber and elsewhere, said Shapiro, who is also an associate professor of medicine at Harvard Medical School. "The data give us confidence to go ahead with testing of cdk inhibitors in combination with DNA-damaging chemotherapy."


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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
Source:Eurekalert

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