Dana-Farber Cancer Institute, Boston, USA.
Cancer Treat Res. 2023;186:171-188. doi: 10.1007/978-3-031-30065-3_10.
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.
具有野生型 BRCA、同源重组功能、或对 PARP 抑制剂的新发或获得性耐药的癌症代表了一个不断增长的患者群体，他们可能受益于联合 PARP 抑制剂策略。我们回顾了血管生成、表观遗传调节剂以及 PI3K、MAPK 和其他细胞信号通路的靶向抑制剂作为同源重组缺陷的诱导剂，为在以前认为不易受 PARP 抑制的情况下使用 PARP 抑制剂提供了支持。
