BRAF

Overview

BRAF is a serine/threonine kinase in the MAPK pathway whose V600E and fusion alterations are among the most therapeutically actionable lesions in oncology.

Alterations observed in the corpus

  • Acquired early in IGHV-mutated CLL but late in IGHV-unmutated CLL by PhylogicNDT temporal ordering (q<0.1) in the 1,148-patient CLL map PMID:35927489.
  • V600E mutations in ~33% of histiocytosis patients profiled in the Make-an-IMPACT direct-to-patient program; BRAF fusions identified including MS4A6A-BRAF, DOCK8-BRAF, and HLA-A-BRAF partners PMID:36862133.
  • One histiocytosis case carried co-occurring KRAS G12D and BRAF D594H PMID:36862133.
  • BRAF alterations were positively associated with SETD2 driver mutations in LUAD (q<0.05) in the MSK-CHORD cohort PMID:39506116.
  • BRAF p.V600E was detected in CSF ctDNA from metastatic melanoma patients; BRAF fusions (including KIAA1549::BRAF) were detected in glioma CSF samples; BRAF fusions also appeared as off-target resistance alterations in EGFR-mutant lung cancer CSF ctDNA in the csf_msk_2024 cohort (1,007 CSF samples, 711 patients) PMID:39289779.
  • BRAF V600E in 21.3% of anaplastic thyroid carcinoma (ATC) vs. 50.9% of papillary thyroid cancer (PTC); clonal/early subclonal timing; mutually exclusive with RAS mutations (multi-omic landscape study, n=87 specimens) PMID:38412093.
  • BRAF oncogenic fusions across 52 histologies (241 fusion-positive tumors from 212 patients); 82 unique 5’ partners including KIAA1549 (25%), SND1 (10%), AGK (6%); de novo prevalence <1% in 69,337 patients; dominant in pilocytic astrocytoma (56% prevalence) PMID:38922339.
  • BRAF fusions are a recurrent (2-4%) mechanism of acquired resistance to EGFR TKIs (osimertinib, erlotinib, afatinib) in lung adenocarcinoma patients in the MSK cohort PMID:38922339.
  • BRAF L597R and G466R pathogenic mutations identified in melanocytes from a tanning cohort donor in a molecular study of indoor tanning effects (182 melanocytes from 26 donors) PMID:38895302.
  • BRAF alterations not independently associated with VTE risk in a 4,141-patient liquid biopsy VTE prediction study PMID:39147831.
  • BRAF oncogenic mutations enriched in early-stage vs late-stage PAAD (3.9% vs 0.7%, p=0.042) but not significant after multiple-comparison correction in a 397-patient sequenced resected PDAC cohort PMID:39214094.
  • BRAF in-frame deletions between N486–P490 found in 7/26 oncogenic BRAF alterations in PAAD — a pattern essentially absent in melanoma (2/749) and thyroid cancer (0/473); one MAPK-WT PDAC tumor harbored a GIT2–BRAF activating fusion in a 2,336-tumor PDAC genomic cohort PMID:39753968.
  • BRAF alterations detected in cfDNA from metastatic urothelial carcinoma patients; numerically higher detection in cfDNA than matched tumor tissue in the CALGB 90601 liquid biopsy cohort (n=200) PMID:40256659.
  • Identified among the significantly mutated genes in 188 primary LUAD tumours (TSP cohort); MAPK pathway member; fell below formal significance threshold in smaller-sample analysis. PMID:18948947
  • Somatic activating mutations in 2 KIT/PDGFRA-wildtype GIST tumors PMID:36593350
  • BRAFK601E detected in CRC PDX; BRAFV600E and BRAF fusions (SEC23A-BRAF) detected in patient ctDNA at resistance to KRASG12C + EGFR inhibition PMID:36355783
  • BRAF alterations assessed in gallbladder carcinoma (GBC) genomic landscape study PMID:36228155
  • BRAF mutation not significantly associated with immunotherapy outcomes in advanced NSCLC (P = 0.80) PMID:36038778
  • Identified as somatically altered in integrative genomic profiling of prostate cancer (MSKCC cohort) PMID:20579941
  • Identified as somatically mutated in TCGA integrated genomic analysis of high-grade serous ovarian carcinoma (HGSOC) PMID:21720365
  • BRAF identified as a recurrently mutated gene in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing of 55 tumors PMID:22343534
  • BRAF inhibitor (PLX4720) sensitivity profiled across cancer cell lines in the Cancer Cell Line Encyclopedia (CCLE), with BRAF V600E as a key pharmacogenomic predictor PMID:22460905
  • V600E hotspot mutation detected in 2 cases of TNBC in a WGS study of 65 breast tumors; noted as clinically actionable PMID:22495314
  • V600E hotspot mutation in 16/25 (64%) melanomas; most significantly mutated gene in a WGS study of 25 melanoma tumors PMID:22622578
  • BRAF is among the significantly mutated genes in colorectal adenocarcinoma across 276 TCGA CRC tumors, with V600E hotspot mutations enriched in the hypermutated microsatellite-unstable subgroup PMID:22810696
  • BRAF (including V600E) is a major driver in melanoma identified by WES of 121 tumors (Broad cohort), occurring in a large fraction of tumors and co-occurring with other driver events PMID:22817889
  • BRAF V600E is the most common driver mutation detected in 147 melanoma tumors (Yale WES cohort), defining the largest molecular subgroup PMID:22842228
  • Mutated in colorectal cancer WES study (Genentech, 74 tumors) PMID:22895193
  • Mutated in TCGA lung squamous cell carcinoma cohort (178 tumors) PMID:22960745
  • Mutated in lung adenocarcinoma WES study (Broad, 183 tumors) PMID:22980975
  • Mutated in breast cancer (TCGA, 510 tumors); BRAF mutations identified in a subset of breast tumors, particularly in the HER2-enriched and luminal B subtypes PMID:23000897
  • MAPK-pathway mutations uncommon in EAC: BRAF mutations absent (0/145 tumors, esca_broad), contrasting with CRC where BRAF mutations are frequent; NF1 mutated in 2% PMID:23525077
  • Activating mutation present in OSCC as part of mitogenic signaling pathway; in CRC, BRAF (not RAS) correlates with CASP8 mutation, suggesting tissue-specific co-mutation patterns (hnsc_mdanderson_2013) PMID:23619168
  • NRF1-BRAF singleton sense-preserving fusion detected in prostate tumor PR-4240 by chromoplexy analysis; BRAF kinase domain left intact, hypothesized to drive overexpression of an oncogenic kinase PMID:23622249
  • Activating fusions in pilocytic astrocytoma: KIAA1549:BRAF in 70/96 cases; novel partners RNF130 (n=2), CLCN6, MKRN1, GNAI1, FAM131B:BRAF; point mutations V600E (n=4), p.ins599T, and novel p.R506_insVLR (interdomain-cleft insertion stabilizing dimerization, matching V600E for ERK phosphorylation) PMID:23817572
  • Mutation in ~2% of high-grade bladder cancers; cited as a validated drug target (analogous to melanoma) within the mutually exclusive MAPK-pathway alteration set (35% combined) PMID:23897969
  • V600E in 5/291 (1.7%) of GBM (TCGA); never co-occurring with NF1 alteration; supports vemurafenib-class therapy in selected GBM patients PMID:24120142
  • V600 missense in 44/45 pre-treatment melanoma tumors; acquired focal amplification in 8.9% of dabrafenib/trametinib-resistant tumors; resistance via MAPK pathway reactivation or bypass mechanisms PMID:24265153
  • Somatic mutation in 3/23 (13%) pancreatic acinar carcinomas, including the V600E oncogenic hotspot; 2/3 mixed acinar-ductal carcinomas carried BRAF mutations; flagged as candidate for BRAF-inhibitor therapy PMID:24293293
  • V600E subclonal in the initial tumor of patient 18 (low-grade glioma) and undetectable in the matched recurrence; the BRAF-mutant clone did not expand despite the typical proliferative advantage of this alteration, demonstrating subclone extinction under treatment PMID:24336570
  • V600E found in 2 atypical sinonasal glands arising in seromucinous hamartoma (ASGSH precursor lesions); these precursor mutations were distinct from mutations in the matched AdCC components PMID:24418857
  • Activating mutations (including non-V600 K601N in U266 cell line and V600E in a clinical case) in multiple myeloma (MM); often subclonal; defines actionable subgroup for BRAF +/- MEK inhibition. BRAF-K601N U266 cells sensitive to PLX4720 and dabrafenib in vitro; combined dabrafenib+trametinib selectively killed BRAF-mutant MM cells PMID:24434212
  • V600E identified in one PAX-fusion-negative rhabdomyosarcoma (RMS) tumor (RMSS013); recurrent in the RAS/MAPK pathway that is mutationally activated in >=45% of PAX-fusion-negative RMS PMID:24436047
  • RAS/RAF/MAPK pathway component; BRAF mutations <5% in HCC but the pathway is universally activated in advanced HCC; cited as resistance analogy (BRAF-mutant melanoma/vemurafenib) motivating combination regimens PMID:24735922
  • Listed among somatic alterations in the HCC molecular landscape (WES, n=1,289); part of the RAF kinase pathway surveyed in the review PMID:24798001
  • Mutations in 10% of LUAD (n=16 cancer-associated activating); represents an oncogenic driver in lung adenocarcinoma across multiple transcriptional subtypes PMID:25079552
  • Driver mutation 100% concordant between primary and metastasis in CRC; trunk event established early in carcinogenesis; concordance supports use of either site for clinical testing to guide cetuximab/panitumumab eligibility PMID:25164765
  • V600 mutation absent in this cSCC cohort (39 patients); referenced as a marker evaluated and not found in cutaneous squamous cell carcinoma PMID:25303977
  • Used as a baseline driver-mutation stratifier in a 128-exome melanoma study of CTLA-4 checkpoint blockade response; BRAF or NRAS mutation status was assessed by cohort arm with no significant enrichment by benefit category claimed PMID:25409260
  • Most common driver in papillary thyroid carcinoma: V600E in 61.7% (248/402) of tumors; BRAF fusions in 13/484 (2.7%) including SND1/BRAF and MKRN1/BRAF; BRAFV600E mutually exclusive with RAS/EIF1AX/fusion-driven cases (p=1.1×10⁻⁵); defines the BVL signaling/differentiation class; associated with older age, higher MACIS scores, and higher risk of recurrence PMID:25417114
  • V600E in 3–7% of intrahepatic CCA and near 0% in extrahepatic CCA; actionable with dabrafenib + trametinib (ROAR phase II ORR ~47% in 43 CCA patients) PMID:25526346
  • Classic CRC driver gene studied as comparison baseline in African American vs. Caucasian CRC cohort; no AA-specific enrichment reported in this study PMID:25583493
  • Non-V600 activating alleles G464R and G469R identified in cutaneous squamous cell carcinoma (29-tumor cSCC NGS cohort); G469R reported in ~1% of BRAF-mutant melanoma PMID:25589618
  • Low-frequency but FDA-druggable alteration in MAP kinase pathway in HCC; part of 243-tumor exome analysis PMID:25822088
  • V600E mutations in 3% of PDA; mutually exclusive with KRAS; patient-derived PDA_014 cell line confirmed vemurafenib-sensitive PMID:25855536
  • Mutations in 10% of PCNSL cases (n=18); identified in genome-wide analysis of primary central nervous system lymphoma PMID:25991819
  • Potentially actionable fusions (BRAF/RAF1) in ~3% of mCRPC patients; identified in integrative genomic analysis of 150 mCRPC biopsies PMID:26000489
  • Mutated in 52% of cutaneous melanoma (V600E n=124, V600K n=18, V600R n=3, K601 n=5); focal amplifications in BRAF subtype; anti-correlated with NRAS hot-spot and NF1 mutations; defines the BRAF-mutant genomic subtype PMID:26091043
  • Mutation in 1/12 (8%) breast adenoid cystic carcinomas; previously reported in 12% (3/25) of an independent breast AdCC cohort; subclonal in at least one case PMID:26095796
  • Rare oncogenic mutation in SCLC (4 tumours total across BRAF/KIT/PIK3CA); kinase-impairing mutations not V600E — suggests targeted therapy potential for rare SCLC subsets PMID:26168399
  • BRAF V600E absent in desmoplastic melanoma; three tumors carry kinase-impaired G466E, G469E, D594N substitutions that paradoxically activate MAPK via CRAF — means standard BRAF V600-directed inhibitors are not applicable PMID:26343386
  • BRAF mutated in 21/538 CLL cases (3.7%) with mutations clustering in the kinase activation segment rather than at V600E, implying a non-canonical activation mechanism and predicted reduced sensitivity to V600E-selective inhibitors (e.g., vemurafenib); BRAF together with NRAS, KRAS, and MAP2K1 account for 8.7% of CLLs with MAPK-ERK pathway mutations PMID:26466571
  • No enrichment of BRAF nonsynonymous mutations was observed between clinical-benefit and no-benefit subgroups in metastatic melanoma patients receiving ipilimumab (CTLA-4 blockade), despite prior reports linking BRAF status to immune-therapy response PMID:26359337
  • 2.4% mutation rate in primary prostate cancer (higher than previously reported); 8 mutations, none V600E; includes K601E, G469A, L597R (MEK-inhibitor sensitive), K601 in-frame deletion, F468C; MAPK-pathway actionable PMID:26544944
  • p.Lys601Glu activating mutation in a CD30-negative CTCL (Sézary syndrome) sample; MEK-pathway convergence across CTCL subtypes PMID:26551667
  • MAPK-pathway alteration enriched in PA-like IDH-wildtype LGG (52%) and LGm6-GBM (32%) in a 1,122-tumour TCGA pan-glioma cohort; BRAF alterations nominate candidate targeted therapies for this favourable-prognosis IDH-wildtype LGG subset PMID:26824661
  • BRAF V600E in 33% PDTC and 45% ATC (n=117 advanced thyroid tumors); BRAF-mutant PDTCs were smaller, more often nodal-metastatic, and overrepresented in females (P = 0.005); 81% of BRAF-mutant PDTCs classified as PDTC only by MSKCC (not Turin) criteria; BRAF co-occurs with TERT promoter mutations (OR 3.4, P = 0.004) PMID:26878173
  • BRAF V600-mutant melanoma cohort used as cross-validation cohort 3 for IPRES resistance signature; prior/concurrent MAPK inhibitor therapy may induce IPRES-overlapping transcriptional programs, potentially compromising subsequent anti-PD-1 response PMID:26997480
  • BRAF p.G466V identified as a recurrent neoepitope hotspot in lung cancer; candidate shared neoantigen for off-the-shelf vaccine design PMID:27158780
  • Classical hotspot activating mutations observed at low frequency in breast cancer (one BRAF V600E in ER- tumour); did not meet Mut-driver criteria as a standalone breast-cancer event in the 2,433-sample METABRIC cohort PMID:27161491
  • BRAF: lower frequency in young lung cancer compared to older patients; MET exon 14 skipping also age-skewed PMID:27346245
  • BRAF: mutated in 1% (n=9) of AML cases; independently adverse (P=0.009, q=0.06); proposed candidate for BRAF inhibitor therapy PMID:27276561
  • BRAF: 3 hotspot mutations (D594N, D594G, G466E) in germ cell tumor cohort (1.7% rate); sorafenib nominated as therapeutic option PMID:27646943
  • BRAF Y472C pathogenic mutation found in a single uRCC case (T69), suggesting overlap with papillary RCC and providing a candidate therapeutic target PMID:27713405
  • TMEM106B-BRAF fusion identified in pleiomorphic xanthoastrocytoma (PXA); classified as a MEK-inhibitor target in the PIPseq pediatric precision-oncology cohort PMID:28007021
  • BRAF is each more frequently mutated in HR+ metastatic breast cancer (mBC) vs primary breast cancer at FDR<0.1; potentially actionable but functional consequences not established PMID:28027327
  • BRAF referenced in the TCGA multi-platform esophageal carcinoma study context; FDA-approved targeted therapies are noted as available for BRAF-mutant tumors in comparison with other MAPK-pathway driver genes profiled in the study PMID:28052061
  • Somatic BRAF p.G469A point mutation and recurrent RUNDC1-BRAF fusion (5.2-fold BRAF overexpression) identified in pheochromocytoma/paraganglioma (PCC/PGL); FDA-approved targeted therapies noted as available for BRAF-mutant tumors PMID:28162975
  • V600E (level 2A) in LUAD: 55.6% matched-therapy uptake, 75% clinical benefit; non-V600E alleles (K601E, D594G, T599dup, SND1-BRAF fusion) had 4/13 matched patients and no clinical benefit; SND1-BRAF fusion treated with BRAF+MEK combo without benefit PMID:28336552
  • V600E (4 patients), V600K+R462K (1), G466E (1) in acral lentiginous melanoma (ALM, n=34); 18% frequency; mutually exclusive of NRAS mutations PMID:28373299
  • V600 mutations detected in >20 tumor types; non-V600 alterations include 33 fusions across 11 tumor types (18 partners; 10 novel) and 7 intragenic multi-exon deletions phenocopying acquired-resistance splice isoforms; CDK5RAP2-BRAF fusion novel in melanoma; 71% radiographic clinical-benefit rate to BRAF-directed therapy in non-melanoma BRAF V600 patients PMID:28481359
  • Activating BRAF fusions identified with novel partners in the MET500 pan-cancer metastatic cohort (500 patients), expanding the targetable fusion landscape beyond canonical contexts PMID:28783718
  • BRAF carries hotspot MAPK-pathway mutations in ~5% of prostate cancer patients alongside HRAS, KRAS, and MAP2K1 PMID:28825054
  • BRAF V600E in 22% of MSI-H vs 5% of MSS mCRC; right-sided enrichment; HR=2.02 for OS. Class 1 (V600), class 2 (RAS-independent dimers), and class 3 (RAS-dependent) mutants all observed; two MSS mCRC cases harbored activating BRAF fusions (AGAP3-BRAF, CUL1-BRAF) PMID:29316426.
  • BRAF mutations observed at low frequency (~2%) in a 240-patient NSCLC ICI cohort; too few events for ICI-response analysis PMID:29337640.
  • BRAF cited as a comparator oncogenic driver with approved targeted therapies achieving higher response rates than neratinib in HER2-mutant disease in the SUMMIT basket trial PMID:29420467.
  • BRAF is among the top recurrent 3’-kinase tyrosine kinases enriched in THCA fusions in a pan-cancer TCGA RNA-seq analysis. PMID:29617662
  • BRAF established hotspot mutations are newly significant in prostate cancer, confirmed in 1,013 prostate cancers (prad_p1000). PMID:29610475

Cancer types (linked)

  • CLL — BRAF is a recurrent driver with subtype-dependent temporal ordering PMID:35927489.
  • Histiocytosis (LCH/ECD) — BRAF V600E is the single most common actionable alteration in the histiocytosis subcohort at 33% PMID:36862133.
  • MEL — BRAF V600E detected in CSF ctDNA from metastatic melanoma patients with CNS involvement; BRAF L597R and G466R mutations found in premalignant melanocytes of tanning bed users PMID:39289779 PMID:38895302.
  • DIFG / glioma — KIAA1549::BRAF fusions detected in glioma CSF ctDNA; 56% prevalence in pilocytic astrocytoma in the tumor-agnostic fusion cohort PMID:39289779 PMID:38922339.
  • NSCLC / LUAD — BRAF fusions as off-target resistance in EGFR-mutant lung cancer; acquired in 10/15 patients with prior EGFR TKI therapy PMID:39289779 PMID:38922339.
  • THPA — BRAF V600E in 21.3% of ATC vs. 50.9% of PTC; early/clonal event mutually exclusive with RAS PMID:38412093.

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • Eight histiocytosis patients with BRAF alterations were treated with vemurafenib or dabrafenib through the Make-an-IMPACT program, contributing to the 17/18 (94%) clinical benefit rate observed with matched targeted therapy PMID:36862133.

Open questions

  • Why BRAF acquisition timing flips between M-CLL (early) and U-CLL (late) is not mechanistically resolved PMID:35927489.

Sources

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