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Article

ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer.

EMBO molecular medicine - 1 Oct 2024

Pozzato Chiara, Outeiro-Pinho Gonçalo, Galiè Mirco, Ramadori Giorgio, Konstantinidou Georgia

Abstract excerpt

Mutated KRAS serves as the oncogenic driver in 30% of non-small cell lung cancers (NSCLCs) and is associated with metastatic and therapy-resistant tumors. Focal Adhesion Kinase (FAK) acts as a mediator in sustaining KRAS-driven lung tumors, and although FAK inhibitors are currently undergoing clinical development, clinical data indicated that their efficacy in producing long-term anti-tumor responses is limited....

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Cyclin-Dependent Kinase 5

Share to Drug Resistance, Neoplasm

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Source

Open in PubMed Open full text

Identifiers

PMID: 39271958
DOI: 10.1038/s44321-024-00138-7
PMCID: PMC11473843

Genes

KRAS
CDK5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer.PMID 39271958Read ↗

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