Kristin Bergethon

TL;DR: Detailed genetic and histological analysis of 37 patients with drug-resistant non–small cell lung cancers carrying EGFR mutations provides new insights into the shifting sands of drug resistance evolution in lung cancers and suggests that serial biopsies may be essential in the quest to reverse or even prevent the development ofdrug resistance.

TL;DR: ROS1 rearrangement defines a molecular subset of NSCLC with distinct clinical characteristics that are similar to those observed in patients with ALK-rearranged NSCLCs, and crizotinib shows in vitro activity and early evidence of clinical activity in ROS1- rearrangedNSCLC.

TL;DR: An NSCLC patient with de novo MET amplification but no ALK rearrangement who achieved a rapid and durable response to crizotinib indicating is also a bona fide MET inhibitor.

TL;DR: MET amplification defines a small and aggressive subset of GEC with indications of transient sensitivity to the targeted MET inhibitor crizotinib (PF-02341066), and survival analysis in patients with stages III and IV disease showed substantially shorter median survival in MET/EGFR-amplified groups.

TL;DR: The mechanisms whereby BRAF-mutant colorectal cancer cells became resistant to a MEK inhibitor were explored and it was discovered that resistance involved amplification of the mutant BRAF gene, implicating BRAF amplification as a mechanism of resistance to both MEK and BRAF inhibitors.