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Changes to DNA on-off switches affect cells' ability to repair breaks, respond to chemotherapy
Date:2/3/2013

tes BRCA1 at a break and the non-homologous end-joining tool repairs the break.

This mechanism can help explain resistance to a promising chemotherapy called PARP inhibition seen in patients and mouse models with BRCA1 mutations. Work from several other research teams surprisingly has shown that if neither BRCA nor 53BP1 are available, then the homologous recombination system goes into action even in the absence of BRCA1 and BRCA1 mutant cancer cells become resistant to PARP inhibitors.

Because of this, Greenberg says, there are some possible applications for making PARP chemotherapy more sensitive: "If you could inhibit specific acetylation events, then a patient's response to PARP inhibitors might be enhanced by hyperactivating 53BP1 binding to breaks in the context of BRCA1 deficient cancers. What's more, measuring the levels of acetylation at H4 might predict how responsive an individual is to PARP inhibitors."

"The story didn't fall into place the way we thought it would," says Greenberg. "We didn't realize that it was a combination of two epigenetic marks that drives the repair system. However, we were able to show that 53BP1 doesn't bind well to regions of histone H4 that are acetylated at a specific location on H4. Collaboration with Georges Mer, a structural biologist at the Mayo Clinic, helped provide the molecular basis for these findings. We think there will be further complexity to this regulation, creating the possibility for the discovery of additional mechanisms that regulate DNA repair pathways and response to therapy and potential new targets for diagnosis and therapy."


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert  

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