Abstract
Poly(ADP-ribose) polymerase (PARP) inhibitors selectively cause the failure of DNA single-stranded break (SSB) repair but do not affect double-stranded break (DSB) repair. Furthermore, antitumor activities have been reported for breast cancer, with germline BRCA1/2 mutations. The prevalence of germline BRCA1/2 mutations never exceed one-tenth; beyond BRCA1/2, genes recurrently altered (more than 5%) in the homologous repair pathway are ARID1A, PALB2, and PTEN. Altered homologous recombination repair genes can total up to one-quarter based on different definitions, and the potential of PARP inhibitors will be elucidated when further studies unraveling the impact of individual homologous recombination genes are conducted.
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