Exploiting Replication Gaps for Cancer Therapy

Overview

Journal Mol Cell

Publisher Cell Press

Specialty Cell Biology

Date 2022 May 14

PMID 35568026

Authors

Ke Cong

Sharon B Cantor

Affiliations

Soon will be listed here.

Abstract

Defects in DNA double-strand break repair are thought to render BRCA1 or BRCA2 (BRCA) mutant tumors selectively sensitive to PARP inhibitors (PARPis). Challenging this framework, BRCA and PARP1 share functions in DNA synthesis on the lagging strand. Thus, BRCA deficiency or "BRCAness" could reflect an inherent lagging strand problem that is vulnerable to drugs such as PARPi that also target the lagging strand, a combination that generates a toxic accumulation of replication gaps.

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