Genetic Information

Gene & Transcript Details

Gene
BRAF
Transcript
NM_001354609.1 MANE Select
Total Exons
Reference Sequence
NC_000007.13
Alternative Transcripts
IDStatusDetails
NM_001354609.2 Alternative 9687 nt | 227–2530
NM_001354609.1 Alternative 9702 nt | 226–2529

Variant Details

HGVS Notation
NM_001354609.1:c.1799T>G
Protein Change
V600G
Location
Exon 15 (Exon 15 of )
15
5'Exon Structure3'
Functional Consequence
Loss of Function
Alternate Identifiers

Clinical & Population Data

Population Frequency

gnomAD
Global Frequency
0.0 in 100,000
Extremely Rare
ACMG Criteria Applied PM2
This variant is absent or extremely rare in population databases (PM2 criteria applies).

ClinVar

Open
Classification
Pathogenic
2 publications
Publications List
PMID: 20735442

The c.1799T>G (p.Val600Gly) variant in BRAF is absent from gnomAD (PM2). It has been identified in one individual with Cardiofaciocutaneous syndrome (PS4_Supporting; PMID: 20735442). It has also been reported in the literature as an unconfirmed de novo occurrence (PM6; GeneDx internal communication). In vitro functional studies provide some evidence that the p.Val600Gly variant may impact protein function (PS3; PMID: 20735442). Furthermore, the variant is in a location that has been defined by the ClinGen RASopathy Expert Panel to be a mutational hotspot or domain of BRAF (PM1; PMID 29493581). Computational prediction tools and conservation analysis suggest that the p.Val600Gly variant may impact the protein (PP3). Finally, the variant is located in BRAF, which has been defined by the ClinGen RASopathy Expert Panel as a gene with a low rate of benign missense variants and pathogenic missense variants are common (PP2; PMID: 29493581). In summary, this variant meets criteria to be classified as pathogenic for RASopathies in an autosomal dominant manner. Rasopathy-specific ACMG/AMP criteria applied (PMID:29493581): PS3, PM1, PM2, PM6, PS4_Supporting, PP3, PP2.

PMID: 20735442

This sequence change replaces valine, which is neutral and non-polar, with glycine, which is neutral and non-polar, at codon 600 of the BRAF protein (p.Val600Gly). This variant is not present in population databases (gnomAD no frequency). This missense change has been observed in individual(s) with cardio-facio-cutaneous syndrome (PMID: 20735442). In at least one individual the variant was observed to be de novo. ClinVar contains an entry for this variant (Variation ID: 40389). Invitae Evidence Modeling incorporating data from in vitro experimental studies (internal data) indicates that this missense variant is expected to disrupt BRAF function with a positive predictive value of 95%. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic.

Clinical Statement

"This variant has been reported in ClinVar as Uncertain significance (1 clinical laboratories) and as Pathogenic (1 clinical laboratories) and as Pathogenic by ClinGen RASopathy Variant Curation Expert Panel expert panel."

COSMIC Somatic Evidence

Open
COSMIC ID
COSM6137
Recurrence
27 occurrences
PM1 Criteria
Applied
COSMIC Database Preview
COSMIC Preview
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Functional Impact & Domains

Functional Domain

Hotspot Status
Not a hotspot
Domain Summary
This variant is not located in a mutational hotspot or critical domain.
Related Variants in This Domain
No evidence of other pathogenic variants at this position in gene BRAF.

Functional Studies & Therapeutic Relevance

Functional Summary

Error in OpenAI Consolidation. OncoKB: BRAFV600GBRAFV600GSomaticNCBI Gene:673|Show additional gene information Variant OverviewBRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others.The BRAF V600G mutation is likely oncogenic.Hide mutation effect description The class I (PMID: 28783719) activating exon 15 BRAF V600G mutation is located in the kinase domain of the protein. This mutation has been found in cardio-facio-cutaneous syndrome (CFC), lung cancer and esophagogastric cancer (PMID: 26287849). Substitutions at position V600 of BRAF, including the common BRAF V600E mutation, are known to be activating and oncogenic (PMID: 12068308, 16273091, 15035987). Expression of this mutation in 293T cells demonstrated that this mutation is activating as measured by increased downstream ERK activation and increased transcription of downstream MAPK pathway transcriptional targets (e.g. ELK) compared to wildtype BRAF (PMID: 20735442). A patient with non-small cell lung cancer (NSCLC) harboring the BRAF V600G mutation had stable disease in response to treatment with vemutafenib, while a patient with sarcoma and a patient with esophagogastric cancer both harboring the BRAF V600G mutation had progressive disease in response to vemurafenib (PMID: 26287849). JAX-CKB: BRAF V600G (previously reported as V599G) lies within the activation segment of the kinase domain of the Braf protein (PMID: 15035987). V600G confers a gain of function to Braf as indicated by increased phosphorylation of BRAF and downstream MEK and ERK and activation of ELK in culture (PMID: 20735442, PMID: 26744778), and in one of two cell lines, increased cell proliferation and viability compared to wild-type Braf (PMID: 29533785).

Database Previews
OncoKB
OncoKB Preview
JAX-CKB
JAX-CKB Preview

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Computational Analysis

Pathogenicity Predictions

SpliceAI
Predictor Consensus
Mixed/VUS
PP3 Applied
No
REVEL Score
0.0
Threshold: ≥0.75 = PP3 applied

SpliceAI Scores

Window: ±500bp
Effect Type Score Position
- Acceptor Loss (AL) 0.07 57 bp
- Donor Loss (DL) 0.11 -61 bp
+ Acceptor Gain (AG) 0.0 0 bp
+ Donor Gain (DG) 0.0 22 bp
High impact (≥0.5) Medium impact (0.2-0.49) Low impact (<0.2)

VCEP Guidelines

Applied ACMG/AMP Criteria (VCEP Specific)

Filter Criteria:
PS3

PS3 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

PM2

PM2 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

PP5

PP5 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

BP4

BP4 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)