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Cited by 138Colorectal Cancer Treatments and StudiesMelanoma and MAPK PathwaysGenetic factors in colorectal cancer

BRAF Mutation in Colorectal Cancer: An Update: Supplementary Issue: Biomarkers for Colon Cancer

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Barras, David·2015·Biomarkers in Cancer
DOI 10.4137/bic.s25248PMC PMC4562608
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Abstract

Colorectal cancer (CRC) is still one of the deadliest cancer-related diseases. About 10% of CRC patients are characterized by a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene resulting in a valine-to-glutamate change at the residue 600 (V600E). This mutation is also present in more than 60% of melanoma patients. BRAF inhibitors were developed and found to improve patient survival; however, most patients at the end of the track ultimately develop resistance to these inhibitors. Melanoma patients benefit from the combination of BRAF inhibitors with mitogen/extracellular signal-regulated kinase (MEK) inhibitors, among others. Unfortunately, colorectal patients do not respond much efficiently, which suggests different resistance mechanisms between the two cancer types. This review aims at shedding light on recent discoveries that improve our understanding of the BRAF mutation biology in CRC.

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  • Activating mutations in BRAF account for around ten to fifteen percent of CRCs, mainly BRAF V600E, a biomarker of poor prognosis.

    “BRAF is a serine/threonine protein kinase (signal transduction protein) and activating mutations in it accounts for around ten to fifteen percent of CRCs, mainly the BRAF V600E—a point mutation and a biomarker of poor prognosis [18,20,21,22].”

    From Overcoming Resistance to Anti-EGFR Therapies: Mechanisms of Cetuximab and Panitumumab Resistance and Emerging Combination Strategies (2026) · cites this paper as [22]

    The Introduction reports BRAF mutations in about 10% of CRC patients, and the BRAF and Mutated BRAF section identifies V600E as the vast majority of BRAF mutations. The Predictive and Prognostic Role section associates BRAF mutation with poorer prognosis. The paper does not give 15% as a CRC estimate; its 15% figure refers to all human cancer types. (LLM, conf=0.82)

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Research works printed but not linked: 36

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Authors
Barras, D.
Affiliations
SIB Swiss Institute of Bioinformatics (CH)
Corresponding author
Barras, David
ORCID
Barras, David
Venue
Biomarkers in Cancer
Publisher
SAGE Publications
Published
2015-01
Volume
7s1
Issue
Suppl 1
Pages
BIC.S25248
ISSN
1179-299X (ISSN-L)
DOI
10.4137/bic.s25248
PMC
PMC4562608
OpenAlex
W2165083157
Cited by
138
References
0
Citations by year
2026: 1 · 2025: 5 · 2024: 7 · 2023: 11 · 2022: 10 · 2021: 10 · 2020: 26 · 2019: 15 · 2018: 12 · 2017: 28 · 2016: 12 · 2015: 1
FWCI
1.90
Type
journal article
Language
en
Open access
Licence
Locations
  • Biomarkers in Cancer (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Keywords
BRAF mutation, colorectal cancer, BRAF V600E mutation, BRAF inhibitors, MEK inhibitors, drug resistance, melanoma, MAPK signaling

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