Mutant RIT1 cooperates with YAP to drive an EMT-like lung cancer state.

ABSTRACT: The discovery of oncogene addiction in cancer has led to the development of over a dozen FDA-approved biomarker-driven therapies in lung adenocarcinoma. Somatic mutations of the "Ras-like in all tissues" (RIT1) gene are non-canonical driver events in lung cancer, occurring in ~2% of lung adenocarcinomas in a mutually exclusive fashion with KRAS and EGFR mutations. Patients with RIT1-mutant lung cancer lack targeted therapy treatment options, and a lack of pre-clinical models has hindered the development of therapeutic strategies for RIT1-mutant lung cancer. Here we report a new mouse model of RIT1-driven lung cancer in which the human RIT1^M90I variant can be induced in a Cre-regulated manner. We show that autochthonous expression of RIT1^M90I

SUBMITTER: Rominger MC 

PROVIDER: S-EPMC11601272 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature