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Article

Cooperative genomic lesions in HRAS-mutant cancers predict resistance to farnesyltransferase inhibitors.

Oncogene - 1 Sept 2024

Nigam Aradhya, Krishnamoorthy Gnana P, Chatila Walid K, Berman Katherine, Saqcena Mahesh, Walch Henry, Venkatramani Mandakini, Ho Alan L, Schultz Nikolaus, Fagin James A, Untch Brian R

Abstract excerpt

In the clinical development of farnesyltransferase inhibitors (FTIs) for HRAS-mutant tumors, responses varied by cancer type. Co-occurring mutations may affect responses. We aimed to uncover cooperative genetic events specific to HRAS-mutant tumors and to study their effect on sensitivity to FTIs. Using targeted sequencing data from the MSK-IMPACT and Dana-Farber Cancer Institute Genomic Evidence Neoplasia...

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Share to Cell Line, Tumor
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 39152269
DOI: 10.1038/s41388-024-03095-0

Genes

HRAS
KRAS
NRAS
BRAF
IMPACT
NF1
PIK3CA
PTEN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

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