Neil Johnson

TL;DR: Dinaciclib augments the degree of response in a PARP-inhibitor-sensitive model, converting tumor growth inhibition to durable regression and support the broad use of combined CDK12 and PARP inhibition in TNBC.

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: Quantitative BRCA1 methylation analysis in a pre-treatment biopsy could allow identification of patients most likely to benefit, and facilitate tailoring of PARPi therapy, as well as identify patients with high-grade serous ovarian carcinoma who respond to the therapy.

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: In this paper, BRCA1-deficient cells have elevated poly(ADP-ribose) and chromatin-associated PARP1, but aberrantly low XRCC1 consistent with defects in backup Okazaki fragment processing (OFP).