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Article

BRAF fusions define a distinct molecular subset of melanomas with potential sensitivity to MEK inhibition.

Clinical cancer research : an official journal of the American Association for Cancer Research - 15 Dec 2013

Hutchinson Katherine E, Lipson Doron, Stephens Philip J, Otto Geoff, Lehmann Brian D, Lyle Pamela L, Vnencak-Jones Cindy L, Ross Jeffrey S, Pietenpol Jennifer A, Sosman Jeffrey A, Puzanov Igor, Miller Vincent A, Pao William

Abstract excerpt

PURPOSE: Recurrent "driver" mutations at specific loci in BRAF, NRAS, KIT, GNAQ, and GNA11 define clinically relevant molecular subsets of melanoma, but more than 30% are "pan-negative" for these recurrent mutations. We sought to identify additional potential drivers in "pan-negative" melanoma. EXPERIMENTAL DESIGN: Using a targeted next-generation sequencing (NGS) assay (FoundationOne™) and targeted RNA...

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Topics

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Share to MAP Kinase Signaling System
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitogen-Activated Protein Kinase Kinases

Share to Multienzyme Complexes

Share to Oncogene Proteins, Fusion

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins B-raf

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Source

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Identifiers

PMID: 24345920
DOI: 10.1158/1078-0432.CCR-13-1746
PMCID: PMC3880773

Genes

BRAF
PAPSS1
TRIM24
GNA11
GNAQ
KIT
NRAS

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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