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Blocking molecular target could make more cancers treatable with PARP inhibitors
Date:6/29/2011

repairing less-serious damage to the DNA strands of cancer cells; if those cells happen to lack a normal BRCA protein, the damage becomes more serious and the cells can't repair it, and then the cells die.

Most types of cancer cells, however, have normal BRCA proteins, making PARP inhibitors less effective. The Dana-Farber scientists sought a way to get around this and convert "BRCA-competent" tumor cells to "BRCA-less" cells that would be sensitive to anti-PARP drugs. Their studies revealed that BRCA1 molecules depend on the cell-cycle protein CDK1 to activate them.

CDK1 was previously identified as a regulator of the cell division cycle that can be overactive in many types of cancers, leading to unchecked growth. Currently several CDK1 inhibitors are in clinical trials as potential weapons against cancer. Shapiro and his colleagues implicated CDK1 for the first time as a control point in the DNA repair circuit that contains BRCA1. This suggested that blocking CDK1 activity might prevent BRCA1 from rescuing cancer cells from life-threatening DNA damage.

In a study involving lung cancer cells in the laboratory and implanted in mice, the researchers "found that if we deplete cancer cells of CDK1, we disrupt DNA repair and the cells become very sensitive to PARP inhibitors," said Shapiro, the senior author of the report. The researchers obtained their results using an existing CDK1- blocking drug along with a PARP inhibitor.

As a more stringent test, they tried the same strategy in mice genetically engineered with an oncogene, KRAS, that drives the most aggressive lung cancers in humans.

"We achieved tremendous responses in this mouse model," Shapiro said. "The survival curve of the animals nearly doubled."

In addition, he said, his team collaborated with pathologists at Brigham and Women's Hospital to show that the CDK1-PARP inhibiting strategy is selective for cancer cells -- normal cells were unaffected. Acco
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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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