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Article

Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer.

Neoplasia (New York, N.Y.) - 1 Mar 2026

Geisen Mariah E, Tessmann Josiane W, Kelson Courtney O, He Daheng, Wang Chi, Faisal Abu Saleh Mosa, Beswick Ellen J, Baca Yasmine, Rock Stephanie, Kolesar Jill M, Zaytseva Yekaterina Y

Abstract excerpt

The presence of BRAFV600E mutations is associated with poor prognosis in colorectal cancer (CRC). Although the FDA-approved combination of encorafenib and cetuximab provides clinical benefit in this population, only 22% of patients respond and most eventually develop resistance. This study investigated the mechanisms of resistance to PLX8394, a second-generation BRAF inhibitor. Using primary and established...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Proto-Oncogene Proteins B-raf

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Source

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Identifiers

PMID: 41650686
DOI: 10.1016/j.neo.2026.101283
PMCID: PMC12906095

Genes

FASN
BRAF
MKI67

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

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Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer.PMID 41650686Read ↗

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