Anwesha Dey

This paper investigates the effects of Hippo pathway inhibition through pharmacological and genetic approaches, identifying kidney, pancreas, and thymus as target organs with dose-dependent toxicities.

The paper identifies synthetic lethality between POLE exonuclease deficiency and high aneuploidy in cancer cells, suggesting POLE inhibition as a therapeutic strategy for aneuploid tumors.

The paper identifies small molecules that induce a cofactor switch in TEAD proteins from YAP to VGLL4, repressing pro-growth gene networks and showing anti-proliferative effects.

This study identifies YAP signaling as a driver of resistance to MEK and AKT inhibitors in NF1-related MPNSTs using preclinical models and spatial transcriptomics.

This study shows that mesothelioma cells develop drug resistance by reverting to a promoter-centric gene regulation mechanism when treated with a TEAD inhibitor.

This study identifies RNF146 as an E3 ubiquitin ligase that degrades TEAD proteins via the proteasome, showing that pharmacological induction of TEAD ubiquitination can suppress YAP/TAZ-driven cancer growth.