Kevin K. Lin

TL;DR: This trial assessed rucaparib versus placebo after response to second-line or later platinum-based chemotherapy in patients with high-grade, recurrent, platinum-sensitive ovarian carcinoma harbouring a BRCA mutation or high percentage of genome-wide loss of heterozygosity.

TL;DR: The ability of tumour genomic LOH, quantified with a next-generation sequencing assay, to predict response to rucaparib, an oral PARP inhibitor, was assessed in ARIEL2, an international, multicentre, two-part, phase 2, open-label study.

TL;DR: CO-1686 is the fi rst drug of its class in clinical development for the treatment of T790M-positive NSCLC, potentially offering potent inhibition of mutant EGFR while avoiding the on-target toxicity observed with inhibition of the WT EGFR.

TL;DR: Evidence is provided for these primary mutations in RAD51C and RAD51D in conferring PARPi sensitivity and secondary mutations as a mechanism of acquired PARPi resistance underpins the need for early delivery of PARPi therapy and for combination strategies.

TL;DR: Targeted next-generation sequencing of circulating cell-free DNA extracted from pretreatment and postprogression plasma in patients with deleterious germline or somatic BRCA mutations treated with the PARP inhibitor rucaparib found BRCa reversion mutations detected in cfDNA from platinum-resistant or platinum-refractory HGOC.