Abstract：
Cancers with wild-type BRCA, homologous recombination proficiency, or de novo or acquired resistance to PARP inhibition represent a growing population of patients who may benefit from combinatorial PARP inhibitor strategies. We review targeted inhibitors of angiogenesis, epigenetic regulators, and PI3K, MAPK, and other cellular signaling pathways as inducers of homologous recombination deficiency, providing support for the use of PARP inhibitors in contexts not previously considered susceptible to PARP inhibition.
摘要：
患有野生型BRCA的癌症，同源重组熟练，或对PARP抑制的从头或获得性耐药代表越来越多的患者可能受益于PARP抑制剂组合策略.我们回顾了血管生成的靶向抑制剂，表观遗传调节因子，PI3K,MAPK,和其他细胞信号通路作为同源重组缺陷的诱导剂，为在以前认为对PARP抑制不敏感的情况下使用PARP抑制剂提供支持。
