IMAGE: By preventing DNA repair, PARP inhibitor drugs cause cancer cells to accumulate mutated chromosomes, ultimately killing them. view more
There is a highly sophisticated way to treat some breast and ovarian cancers–a class of drugs called PARP inhibitors, designed to exploit the very defects that make tumors with certain mutations especially deadly. Yet this targeted approach to cancer therapy sometimes fails, and scientists have anxiously sought to understand why.
Now, research at The Rockefeller University offers insight into the biology behind this drug resistance and fresh hope for fighting it. Scientists in Titia de Lange‘s lab and their colleagues have discovered the molecular means by which some cancers caused by errors in the gene BRCA1 evade treatment by drugs custom-tailored to kill them.
Described in Nature on July 18, their work challenges previous assumptions about the mechanics by which these PARP inhibitors succeed or fail to help patients.
“This is a complete shift in our understanding of the mechanism that underlies this form of treatment for BRCA1 cancers,” says de Lange, the Leon Hess Professor.
Their discovery helps to explain why some cancers respond to PARP inhibitors, while others do not–an insight that could ultimately be used to help
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