A screen was performed to determine what genetic events would allow normal cells to tolerate loss of functional BRCA1. It was found that loss of another DNA repair protein, 53BP1 (p53 Binding Protein 1) allows cells to continue growing after loss of BRCA1. Moreover loss of normal production of the 53BP1 protein was found in a subset of BRCA1-associated cancers and in sporadic "triple-negative" breast cancers in two independent breast cancer patient cohorts from the United States and Finland. According to the investigators, these data suggest that loss of 53BP1 may allow cells to tolerate loss of BRCA1, and that some breast cancers may have acquired loss of 53BP1 protein expression.

CINJ medical oncologist Shridar Ganesan, MD, PhD, assistant professor of medicine and pharmacology at UMDNJ-Robert Wood Johnson Medical School, is one of the senior authors on the study. "Loss of 53BP1 in breast cancer cells may give some clue to their underlying biology, and may ultimately impact their responsiveness to certain chemotherapeutic agents that are being used to treat these aggressive cancers," he noted. "This is especially true regarding platinum-based drugs as well as a new class of agents known as PARP inhibitors, as cancers arising in women with BRCA mutations have been shown to be sensitive to these specific treatments. We hope to ultimately be able to predict why some patients respond well to these treatments and others are resistant. This work was the result of a group effort involving the laboratories of Jos Jonkers, Madelana Tarsounas and Jiri Bartek in Europe, and shows the importance of international collaborations in advancing cancer research."

SOURCE Cancer Institute of New Jersey