Ethan V. Abel

This study identifies sustained cell cycle activity as a mechanism of resistance to KRAS inhibitors and shows that co-targeting cell cycle nodes with CDK4/6 or CDK2 restores sensitivity and provides durable tumor control.

This paper identifies HNF1A as a BRD4 target and shows that BET-inhibitors' antitumor effects in PDAC depend on HNF1A ablation.

This study identifies HNF1A as an oncogenic driver of PDAC metastasis through upregulation of FGFR4 and shows that FGFR4 inhibition reduces metastasis in vitro and in vivo.