Loss of KEAP1 modulates sensitivity to targeted therapies in lung cancer.

Combined EGFR and SOS1 inhibition synergize to inhibit NSCLC spheroid growth.

Cancer cells driven by mutations in KRAS or EGFR are dependent on DUSP6 to prevent ERK-induced cell death, creating a novel vulnerability for targeted therapy.

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

Targeted therapies induce an aberrant fucosylation of complex tumor secretomes stimulating the expansion of minority drug-resistant clones and promoting therapy resistance.

A new luciferase and fluorescent reporter system enables rapid and efficient in-cell profiling of the majority of protein kinase oncogenes known to date.

Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.

The combination of ceritinib with CGM097 demonstrates remarkable antitumor activity in TP53 wild-type neuroblastoma models with ALK aberrations and is able to overcome the resistance acquired during ceritinib treatment.