Yifan Wang

TL;DR: Evidence is provided for a two-event mechanism by which BRCA1-mutant tumors acquire anticancer therapy resistance by involving heat shock protein (HSP)90-mediated stabilization of a BRCT domain mutant BRCa1 protein under PARP inhibitor selection pressure.

TL;DR: Evidence is provided that cancer cells employ a strategy to remove deleterious germline BRCA1 mutations through alternative mRNA splicing, giving rise to isoforms that retain residual activity and contribute to therapeutic resistance.

TL;DR: The authors show that the combination of PARP and ATR inhibitors increases the therapeutic response in PAR Pi and platinum resistant ovarium cancer PDX models, indicating that PARPi-ATRi is a highly promising strategy for OVCAs that acquire resistance to PARPi and platinum.

TL;DR: Results indicate that RING-deficient BRCA1 proteins are hypomorphic and capable of contributing to PARPi and platinum resistance when expressed at high levels.

TL;DR: It is shown that the E3 ubiquitin ligase RNF168, in addition to its canonical role in inhibiting end resection, acts in a redundant manner with BRCA1 to load PALB2 onto damaged DNA.