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The RAC1 P29S hotspot mutation in melanoma confers resistance to pharmacological inhibition of RAF.

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Cancer Res2014PMID 25056119PMC4167745stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (5)

How each link was made (MeSH, dictionary, registry reference, curation…) and whether it has been validated. Candidate links are not counted in entity statistics.

Validated 5

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
25056119
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
RAC1 P29S1
Dabrafenib + VemurafenibSubstitutesMelanomaPredictiveDSupports Resistance4accepted
EID873

Melanoma cell lines harboring the RAC1 P29S hotspot mutation were shown to be resistant to BRAF inhibition with vemurafenib or dabrafenib and knock-in or knock-out of this mutation decreased and incre… (full text at CIViC)

PMID 25056119 · Watson et al., 2014 · Open in CIViC

civic