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Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy.

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Pigment Cell Melanoma Res2013PMID 23890088PMC3808507stubpubmedProvenance
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 (2)

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
23890088
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–2 of 2 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
BRAF Fusion2
SorafenibMelanomaPredictiveCSupports Sensitivity Response2accepted
EID723

BRAF fusion AGK-BRAF was associated with decreased sensitivity to vemurafenib and increased sensitivity to sorafenib in-vitro. A single patient with this fusion showed durable response to sorafenib.

PMID 23890088 · Botton et al., 2013 · Open in CIViC

civic
VemurafenibMelanomaPredictiveDSupports Resistance2accepted
EID724

A melanoma cell line with AGK-BRAF in-frame fusion showed decreased sensitivity towards Vemurafenib in comparison with BRAF mutated (V600E) cell lines.

PMID 23890088 · Botton et al., 2013 · Open in CIViC

civic