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Andrew J. Armstrong, MD, discusses the utility of PARP inhibitors in mutated prostate cancer.
Andrew J. Armstrong, MD, professor of medicine, associate professor in pharmacology and cancer biology, and professor in surgery at Duke University School of Medicine; and member of the Duke Cancer Institute, discusses the utility of PARP inhibitors in mutated prostate cancer.
Not all patients with prostate cancer who have BRCA2 mutations have DNA repair defects and only about half of those patients respond to PARP inhibitors, says Armstrong. Other patients, for example, with ATM mutations, may not respond to a PARP inhibitor either and it is generally felt that the patients who are more likely to respond to a PARP inhibitor have a lot of DNA damage across their genome and DNA repair defects, adds Armstrong. The phenotype that The Expanded Prostate Cancer Index Composite is using will, ideally, capture those patients who may have other DNA repair defects beyond the homologous repair mutation, such as epigenetic silencing. It is hopeful that it may expand the group of patients with prostate cancer that could respond to PARP inhibition, concludes Armstrong.