The ERBB network facilitates KRAS-driven lung tumorigenesis.

ABSTRACT: KRAS is the most frequently mutated driver oncogene in human adenocarcinoma of the lung. There are presently no clinically proven strategies for treatment of KRAS-driven lung cancer. Activating mutations in KRAS are thought to confer independence from upstream signaling; however, recent data suggest that this independence may not be absolute. We show that initiation and progression of KRAS-driven lung tumors require input from ERBB family receptor tyrosine kinases (RTKs): Multiple ERBB RTKs are expressed and active from the earliest stages of KRAS-driven lung tumor development, and treatment with a multi-ERBB inhibitor suppresses formation of KRAS^G12D-driven lung tumors. We present evidence that ERBB activity amplifies signaling through the core RAS pathway, supporting prolifera

SUBMITTER: Kruspig B 

PROVIDER: S-EPMC6881183 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature