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BRAF (v-raf murine sarcoma viral oncogene homolog B1)

Written2020-05Enric Domingo
Department of Oncology, University of Oxford, Oxford, United Kingdom / enric.domingo@oncology.ox.ac.uk
This article is an update of :
2004-09Enric Domingo, Simo Schwartz Jr
Oncologia Molecular i Envelliment, Centre d'Investigacions en Bioqumica i Biologia Molecular (CIBBIM) Hospital Universitari Vall d'Hebron Passeig Vall d'Hebron 119-129 Barcelona 08035, Catalonia, Spain

Abstract Review on BRAF, with data on DNA, on the protein encoded, and where the gene is implicated.

Keywords serine/threonine kinase; RAS/RAF/MAPK pathway; mitogenic signals; Ras proteins

(Note : for Links provided by Atlas : click)

Identity

Alias (NCBI)v-raf murine sarcoma viral oncogene homolog B1
BRAF1
RAFB1
NS7
HGNC (Hugo) BRAF
HGNC Alias symbBRAF1
HGNC Previous namev-raf murine sarcoma viral oncogene homolog B
LocusID (NCBI) 673
Atlas_Id 828
Location 7q34  [Link to chromosome band 7q34]
Location_base_pair Starts at 140730665 and ends at 140924929 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping BRAF.png]
Local_order Between the NDUFB2 and MRPS33 genes.
 
  Probe(s) - Courtesy Mariano Rocchi, Resources for Molecular Cytogenetics
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
AGAP3 (7q36.1)::BRAF (7q34)AGK (7q34)::BRAF (7q34)AGTRAP (1p36.22)::BRAF (7q34)
AKAP9 (7q21.2)::BRAF (7q34)AP3B1 (5q14.1)::BRAF (7q34)ARMC10 (7q22.1)::BRAF (7q34)
ATG7 (3p25.3)::BRAF (7q34)BCL2L11 (2q13)::BRAF (7q34)BRAF (7q34)::AGK (7q34)
BRAF (7q34)::AKAP9 (7q21.2)BRAF (7q34)::AP3B1 (5q14.1)BRAF (7q34)::ATG7 (3p25.3)
BRAF (7q34)::BRAF (7q34)BRAF (7q34)::CIITA (16p13.13)BRAF (7q34)::FAM114A2 (5q33.2)
BRAF (7q34)::HIBADH (7p15.2)BRAF (7q34)::KIAA1549 (7q34)BRAF (7q34)::MACF1 (1p34.3)
BRAF (7q34)::MRPS33 (7q34)BRAF (7q34)::SLC26A4 (7q22.3)BRAF (7q34)::SND1 (7q32.1)
BRAF (7q34)::SUGCT (7p14.1)BTF3L4 (1p32.3)::BRAF (7q34)CCDC6 (10q21.2)::BRAF (7q34)
CCDC91 (12p11.22)::BRAF (7q34)CCNY (10p11.21)::BRAF (7q34)CDC27 (17q21.32)::BRAF (7q34)
CEP89 (19q13.11)::BRAF (7q34)CLCN6 (1p36.22)::BRAF (7q34)CUL1 (7q36.1)::BRAF (7q34)
CUX1 (7q22.1)::BRAF (7q34)DYNC1I2 (2q31.1)::BRAF (7q34)EPS15 (1p32.3)::BRAF (7q34)
ERC1 (12p13.33)::BRAF (7q34)ETFA (15q24.2)::BRAF (7q34)FAM114A2 (5q33.2)::BRAF (7q34)
FAM131B (7q34)::BRAF (7q34)FCHSD1 (5q31.3)::BRAF (7q34)FXR1 (3q26.33)::BRAF (7q34)
GATM (15q21.1)::BRAF (7q34)GHR (5p13.1)::BRAF (7q34)GNAI1 (7q21.11)::BRAF (7q34)
GTF2I (7q11.23)::BRAF (7q34)HERPUD1 (16q13)::BRAF (7q34)HIBADH (7p15.2)::BRAF (7q34)
KDM7A (7q34)::BRAF (7q34)KIAA1549 (7q34)::BRAF (7q34)KLHL7 (7p15.3)::BRAF (7q34)
LSM14A (19q13.11)::BRAF (7q34)MACF1 (1p34.3)::BRAF (7q34)MKRN1 (7q34)::BRAF (7q34)
MYRIP (3p22.1)::BRAF (7q34)MZT1 (13q21.33)::BRAF (7q34)NRF1 (7q32.2)::BRAF (7q34)
NUB1 (7q36.1)::BRAF (7q34)NUP214 (9q34.13)::BRAF (7q34)RAD18 (3p25.3)::BRAF (7q34)
RBMS3 (3p24.1)::BRAF (7q34)RNF130 (5q35.3)::BRAF (7q34)SLC12A7 (5p15.33)::BRAF (7q34)
SLC45A3 (1q32.1)::BRAF (7q34)SND1 (7q32.1)::BRAF (7q34)STMP1 (7q33)::BRAF (7q34)
TANK (2q24.2)::BRAF (7q34)TAX1BP1 (7p15.2)::BRAF (7q34)TRIM24 (7q33)::BRAF (7q34)
ZC3HAV1 (7q34)::BRAF (7q34)ZKSCAN1 (7q22.1)::BRAF (7q34)ZNF767P (7q36.1)::BRAF (7q34)
ZSCAN30 (18q12.2)::BRAF (7q34)

DNA/RNA

Description The main isoform of the BRAF gene (NM_004333) is composed of 18 exons spanning in a region of 205601 bp.
Transcription The main transcript NM_004333 has 6459 bp.
Pseudogene BRAFP1 (alias BRAF2) in Xq13.3

Protein

Note The real sequence A31 G32 A33 was erroneously considered R31 P32. As the A33 was missing in previous sequences, some articles have erroneously assigned wrong numbers to coding mutations and amino acids (i.e. V599E mutation instead of V600E).
 
  Figure 1. Diagram of the BRAF protein in scale. Numbers inside the blue boxes indicate the exon from which is translated each part of the protein. The three boxes inside represent the conserved regions of the protein with the ARAF and RAF1 genes (CR1, CR2 and CR3). With green bars are represented three different domains: RBD (Ras binding domain), CRD (Cysteine-rich domain) and KD (Kinase domain). A conserved glycine motif (G-loop) in exon 11 is indicated with a red bar and the activation segment (AS) in exon 15 with a pink bar. The black arrows indicate the major phosphorylation sites of the protein. C: Carboxyl-terminal; N: Amino-terminal.
Description Amino acids: 766. Molecular Weight: 84437 Daltons. The BRAF gene is a proto-oncogene that belongs to the Serine/Threonine Kinase Family. It is also a member of the RAF Subfamily together with the ARAF and RAF1 genes.
Expression BRAF is expressed in most tissues. Protein expression using antibody staining is not mainly consistent with RNA expression.
Localisation Cytoplasmic.
Function BRAF is a serine/threonine kinase that belongs to the RAS/RAF/MEK/ERK/MAPK pathway, which is involved in the transduction of mitogenic signals from the cell membrane to the nucleus. BRAF in its inactive form has region CR1 autoinhibiting region CR3 that contains the Kinase Domain, preventing BRAF kinase abilities. The activated form of BRAF is triggered by Ras proteins. RAS is inactive when bound to GDP, but when it binds to GTP becomes active and promotes phosphorylation and activation of BRAF and the pathway signal. This step is mediated by the Ras Binding Domain (RBD) in CR1 of BRAF, which is released ceasing the kinase inhibition. Several downstream genes have been found to be activated by this pathway, among them, CCND1 (cyclin D1), CCND2 ( cyclin D2) and CCND3 (cyclin D3) (self-sufficiency in growth), VEGF (angiogenesis), MYC (insensitivity to antigrowth signals), ITGB3 (b3-integrin )(tissue invasion and metastasis) and MDM2 (apoptosis evasion, limitless replicative potential and angiogenesis).
Homology BRAF shares three conserved regions (CR1, CR2 and CR3) with the other two RAF genes: ARAF and RAF1 (Figure 1). CR1, which has 131 aa, contains the cysteine-rich domain (CRD) and most of the Ras binding domain (RBD). These two domains bind to RAS-GTP. CR2, which has 16 aa, is rich in serine and threonine residues, including S365 as an inhibitory phosphorylation site. Finally CR3, which has 293 aa and has the kinase domain, contains also the G-loop GXGXXG motif (highly conserved in most of the human kinases), the activation segment and the regulatory phosphorylation sites S446, S447, D448, D449, T599 and S602. The other two RAF genes do not show pathogenic mutations for unclear reasons.

Mutations

Note BRAF contains several single nucleotide polymorphisms, both synonymous and non-synonymous. It is unclear whether any of them may impact BRAF function.
 
  Figure 2. Frequency of BRAF mutations in several tumour types. Data and plot taken from pancancer TCGA in cbioportal.
 
  Figure 3. Somatic mutations found in BRAF (taken from cbioportal). The low panel shows the same data decreasing the highest mutation number to better visualise atypical BRAF mutations. Location of cancer hotspot mutations are show in the line below.
 
  Figure 4. Mutations in BRAF, KRAS, NRAS and HRAS genes do not overlap (taken from cbioportal).
Epigenetics BRAF has some CpG sites from upstream the transcription start site to the first exon but no methylation has ever been described.
Germinal No germinal mutations described. BRAF germline mutations result in a large proportion of cardiofaciocutaneous syndrome cases, a rare but serious genetic disorder characterised by distinctive craniofacial malformations. A few other germline mutations in BRAF have also been described in similar developmental disorders like Costello, Noonan or Leopard syndromes. These germline mutations are mostly located in exons 6, 12, 15 and 16 affecting residues in the Cysteine-rich or Kinase domains. They have minimal overlap with somatic mutations described in cancer. In addition, carriers of these germline mutations do not seem to show high risk of developing cancer.
Somatic BRAF presents somatic mutations in different sort of tumours like thyroid cancer, malignant melanoma, sporadic colorectal tumors showing mismatch repair defects in microsatellites (MSI) and low-grade ovarian serous carcinoma (Figure 2). A majority of these mutations correspond to the hotspot transversion mutation T1799A that causes the amino acidic substitution V600E, which is the most common single nucleotide change in cancer (Figure 3a). The other atypical ones account for a wide variable range of missense mutations residing in the glycines of the G-loop in exon 11 or in the activation segment in exon 15 near the V600 residue (Figure 3b). The mutation V600E confers transformant activity to the cells because it mimics the phosphorylation of T599 and/or S602 in the activation segment so BRAF rests constitutively active in a RAS independent manner.
BRAF mutations can be classified into 3 subtypes depending on their effect on BRAF activity. Class 1 mutations function as an active monomer and are Ras-independent as they do not require any upstream signaling from Ras. Mutations in codon 600 like the main hotspot are examples of Class 1 mutations. Class 2 mutations are also Ras-independent but they act as dimers (eg K601E, K601N, K601T, L597Q, L597V, G469A, G469V, G469R, G464V). Class 3 are mutations that inactivate the kinase domain but strikingly result in higher MAPK signalling. This is because these are Ras-dependent mutations that also provide higher affinity to both Ras and RAF1 (CRAF), resulting in increased downstream signalling. Examples of Class 3 mutations are D287H, V459L, G466V, G466E, G466A, S467L, G469E, N581S, N581I, D594N, D594G, D594A, D594H, F595L, G596D.
Mutations in the Ras genes HRAS, KRAS or NRAS are not concomitant with BRAF mutations (Figure 4), strongly suggesting same pathway activation. The exception are Class 3 BRAF mutations, probably because they benefit from upstream pathway overactivation by Ras mutations.
BRAF-V600E is not present in other tumours like high-grade ovarian serous carcinoma, gastric cancer, esophageal cancer, endometrial cancer, uveal melanoma, biliary tract cancer or hepatocellular carcinoma.. Gene fusions retaining an intact kinase domain of BRAF have been found in different tumour types at frequencies below 3%.

Implicated in

Note
  
Entity Melanoma
Note BRAF is mutated in about 60% of malignant melanomas. The mutation V600E is an early event and an oncogenic driver upregulating cellular proliferation. However, BRAF V600E alone is insufficient for the development of melanoma as it is present in 80% of benign and dysplastic melanocytic nevi, which are the first lesions associated with this tumour type. Other alterations might be required to induce malignant transformation. No BRAF mutations are associated with uveal melanoma.
BRAF mutations in melanoma are associated with younger age at diagnosis, superficial spreading or nodular histology, anatomical regions without chronic sun damage and higher chances to metastasise to the brain.
Prognosis Metastatic melanoma patients with mutations in BRAF show worse overall survival than BRAF wild types. BRAF inhibition has also been tested to treat melanoma patients given the relevance of MAPK pathway and the high frequency of BRAF mutations. As a result, some BRAF inhibitors have been implemented clinically and have improved outcome recently in melanoma. Sorafenib is a multitargeted tyrosine kinase inhibitor for different genes including BRAF (wild type and mutant) and RAF1 (CRAF). However, several studies found it ineffective in melanoma both as single agent or combined with cytotoxic chemotherapy. However, vemurafenib (for V600E mutated BRAF inhibition) is an inhibitor specific for BRAF V600E (and also V600K) that proved to increase survival and response rates. More recently, it has been shown that the combination of BRAF and MEK inhibitors (eg dabrafenib + trametinib or vemurafenib + cobimetinib) provides even better outcomes as it better prevents resistance compared to BRAF inhibition monotherapy. These combinational treatments are currently used as part of the standard of care of BRAF mutant melanoma patients, usually when they are advanced, metastatic or unresectable. Nevertheless, resistance may eventually occur by both unknown and known molecular alterations (eg recovery of MAPK signaling by secondary Ras/Raf mutations, BRAF amplification or changes in RNA expression).
  
  
Entity Colorectal cancer
Note BRAF mutation V600E is associated with mismatch repair deficiency (MSI) and found in 40% of the cases while in mismatch repair proficient tumors (MSS) the frequency is around 5%. Gastric and endometrial MSI and MSS tumors do not have BRAF mutations. In sporadic MSI colon cases this mutation is found in proximal colon tumors with MLH1 methylation (80% of cases), while in tumors from the hereditary nonpolyposis colorectal cancer (HNPCC), either with MLH1, MSH2 or MSH6 germline mutations or none, no BRAF mutations are detected. Because of this BRAF V600E mutation is used for HNPCC diagnostic as an exclusion criteria for germline mutation in mismatch repair genes. BRAF V600E associations with MLH1 methylation and MSI are secondary to the main association with CpG Island Methylator Phenotype (CIMP), a form of genome-wide global methylation. These are common features in sessile serrated adenomas, strongly suggesting these may be the precursors of their counterparts in colorectal carcinomas. Due to strong association with MSI, BRAF V600E is also associated with older age, female gender, poor differentiation and mucinous phenotype. The primary reasons for all these associations are unclear. Interestingly, they do not seem to have been identified in other tumour types.
Recently, it has been suggested that BRAF V600E colorectal cancers may be classified in two distinct subtypes based on their RNA expression patterns: BM1 (KRAS/AKT pathway activation, mTOR/4EBP deregulation, epithelial-mesenchymal transition) and BM2 (cell cycle deregulation).
Prognosis Due to its high association with MSI, a very well-known biomarker for good prognosis, BRAF V600E mutation is more frequent in stages I/II/III (about 10%) than in stage IV (about 5%). However, BRAF V600E mutation provides poor prognosis in the metastatic setting and also in the subset of MSS patients in stage III. This may be due to chemoresistance in these patients routinely treated with adjuvant cytotoxic chemotherapy. Strikingly, BRAF mutations have been linked to nodal and peritoneal metastases but not to lung or liver metastases, suggesting specific biological behavior depending on BRAF status. Surprisingly, atypical non-V600E BRAF mutations may provide longer overall survival than both BRAF-V600E mutants and wild types in the metastatic setting.
Although mutations in the upstream genes KRAS and NRAS are good biomarkers for lack of response to EGFR inhibition, BRAF V600E mutation does not seem to provide such information. Conversely, atypical non-V600E BRAF mutations do seem to be associated with resistance to EGFR inhibition.
Unlike melanoma, BRAF inhibitors in colorectal cancer have not proved to be effective due to rapid feedback activation of the EGFR pathway by a wide range of different molecular alterations. However, the first results of the BEACON clinical trial suggest that combining encorafenib (BRAF inhibitor) and cetuximab (EGFR inhibitor) with or without binimetinib (MEK inhibitor) may improve response and survival than standard therapy in BRAF-V600E metastatic colorectal cancer patients.
  
  
Entity Ovarian cancer
Note The only BRAF mutation is V600E which is found in 30% of low-grade serous carcinoma and borderline tumors. The mutation seems to occur very early in the development. High-grade tumors do not show BRAF mutations.
Prognosis There is evidence that BRAF mutation provides good prognosis in early stage low-grade serous ovarian cancer.
  
  
Entity Thyroid cancer
Note In thyroid papillary cancer the only BRAF mutation present is V600E with a frequency around 60%, making it the most common molecular alteration of this tumour type. The K601E mutation has also been found in some cases of the follicular variant of thyroid cancer.
Prognosis In thyroid papillary cancer BRAF V600E mutation is associated with advanced tumour stage at diagnosis, lymph nodes, distant metastases, high rate of recurrence and shorter overall and disease-free survival. However, it has been suggested it may not be an independent biomarker of poor outcome and its effect should be put in context with other prognostic factors.
Inhibition of BRAF by two multikinase inhibitors, sorafenib and levantinib, are established therapeutic options for papillary thyroid tumours refractory to radioiodine therapy. Single agent inhibition specific for BRAF V600E mutation by vemurafenib and dabrafenib is not used as the clinical benefit was not considered reasonable compared to the toxicity provided. These two agents improved progression free survival but did not have much effect on overall survival. Several clinical trials are underway testing different combinations of BRAF inhibition with other agents targeting pathways related with resistance.
  
  
Entity Non-Small Cell Lung cancer
Note This tumour type shows a modest frequency of BRAF mutations (1-4%). Unlike all the other tumour types, atypical BRAF mutations account for half of all BRAF mutations, the other half being V600E mutations.
Prognosis BRAF V600E mutation is a marker for worse prognosis in patients treated with platinum-based agents. This outcome is consistent with chemoresistance as suggested in other tumour types. Similarly, dual inhibition of BRAF and MEK by dabrafenib and trametinib respectively improves outcome compared to standard chemotherapy and single agent BRAF inhibition.
  
  
Entity cell lines
Note Table 1. BRAF mutational status in cell lines from colorectal, ovarian, skin, thyroid and lung cancer. Data taken from the Cancer Cell Line Encyclopedia in April 2020.
TISSUE TYPECELL LINEBRAF MUTTISSUE TYPECELL LINEBRAF MUT
LARGE INTESTINESNU503D22NLUNGISTSL2X203_splice
LARGE INTESTINESNUC4D22NLUNGHCC1588E204L
LARGE INTESTINESNU1040V120I S76PLUNGNCIH2227A320S
LARGE INTESTINELS513E204L E204V E204*LUNGT3M10I326V
LARGE INTESTINELS180D211GLUNGNCIH1651E375D
LARGE INTESTINECCK81S273N R506GLUNGRERFLCAD1R435S
LARGE INTESTINEHT115R354QLUNGCAL12TG466V
LARGE INTESTINEKM12A712T A404Cfs*9LUNGNCIH1666G466V
LARGE INTESTINEGP2DT529ALUNGNCIH1395G469A
LARGE INTESTINEGP5DT529ALUNGNCIH1755G469A
LARGE INTESTINEHT55N581YLUNGNCIH2405L485_P490delinsF P490Yfs*11 L485Yfs*14
LARGE INTESTINENCIH508G596RLUNGNCIH2087L597V
LARGE INTESTINECL34V600ELUNGHCC364V600E
LARGE INTESTINECOLO201V600ELUNGNCIH854V600E
LARGE INTESTINECOLO205V600ELUNGSW1271S683N
LARGE INTESTINELS411NV600ELUNG201TWT
LARGE INTESTINERKOV600ELUNGA427WT
LARGE INTESTINESNUC5V600ELUNGA549WT
LARGE INTESTINEHT29V600E T119SLUNGBENWT
LARGE INTESTINEMDST8V600E V600K V600MLUNGCALU1WT
LARGE INTESTINEOUMS23V600E X287_spliceLUNGCALU3WT
LARGE INTESTINESNU407R726CLUNGCALU6WT
LARGE INTESTINEC10WTLUNGCHAGOK1WT
LARGE INTESTINEC125PMWTLUNGCOLO668WT
LARGE INTESTINEC2BBE1WTLUNGCOLO699WT
LARGE INTESTINEC75WTLUNGCORL105WT
LARGE INTESTINEC80WTLUNGCORL23WT
LARGE INTESTINEC84WTLUNGCORL24WT
LARGE INTESTINEC99WTLUNGCORL279WT
LARGE INTESTINECACO2WTLUNGCORL303WT
LARGE INTESTINECAR1WTLUNGCORL311WT
LARGE INTESTINECL11WTLUNGCORL32WT
LARGE INTESTINECL14WTLUNGCORL47WT
LARGE INTESTINECL40WTLUNGCORL51WT
LARGE INTESTINECOLO320WTLUNGCORL88WT
LARGE INTESTINECOLO678WTLUNGCORL95WT
LARGE INTESTINECW2WTLUNGCPCNWT
LARGE INTESTINEDIFIWTLUNGDMS114WT
LARGE INTESTINEGEOWTLUNGDMS153WT
LARGE INTESTINEHCC2998WTLUNGDMS273WT
LARGE INTESTINEHCC56WTLUNGDMS454WT
LARGE INTESTINEHCT116WTLUNGDMS53WT
LARGE INTESTINEHCT15WTLUNGDMS79WT
LARGE INTESTINEHRT18WTLUNGDV90WT
LARGE INTESTINELIM1215WTLUNGEBC1WT
LARGE INTESTINELOVOWTLUNGEKVXWT
LARGE INTESTINELS1034WTLUNGEMCBAC1WT
LARGE INTESTINELS123WTLUNGEMCBAC2WT
LARGE INTESTINENCIH630WTLUNGEPLC272HWT
LARGE INTESTINENCIH716WTLUNGHARAWT
LARGE INTESTINENCIH747WTLUNGHCC1171WT
LARGE INTESTINERCM1WTLUNGHCC1195WT
LARGE INTESTINESKCO1WTLUNGHCC1359WT
LARGE INTESTINESNU1033WTLUNGHCC1438WT
LARGE INTESTINESNU1197WTLUNGHCC15WT
LARGE INTESTINESNU175WTLUNGHCC1833WT
LARGE INTESTINESNU283WTLUNGHCC2108WT
LARGE INTESTINESNU61WTLUNGHCC2279WT
LARGE INTESTINESNU81WTLUNGHCC2429WT
LARGE INTESTINESNUC1WTLUNGHCC2450WT
LARGE INTESTINESNUC2AWTLUNGHCC2814WT
LARGE INTESTINESNUC2BWTLUNGHCC2935WT
LARGE INTESTINESW1116WTLUNGHCC33WT
LARGE INTESTINESW1463WTLUNGHCC366WT
LARGE INTESTINESW403WTLUNGHCC4006WT
LARGE INTESTINESW48WTLUNGHCC44WT
LARGE INTESTINESW480WTLUNGHCC461WT
LARGE INTESTINESW620WTLUNGHCC515WT
LARGE INTESTINESW837WTLUNGHCC78WT
LARGE INTESTINESW948WTLUNGHCC827WT
LARGE INTESTINET84WTLUNGHCC827GR5WT
OVARYA2780V226MLUNGHCC95WT
OVARYOC314P403Lfs*8 A747VLUNGHOP62WT
OVARYOC316P403Lfs*8 A747VLUNGHOP92WT
OVARYHEYG464ELUNGIALMWT
OVARYHEYA8G464ELUNGISTSL1WT
OVARYOV90N486_P490delLUNGJHU028WT
OVARYES2V600ELUNGKNS62WT
OVARYJHOM2BV600ELUNGLB647SCLCWT
OVARY59MWTLUNGLC1FWT
OVARYBIN67WTLUNGLC1SQWT
OVARYCAOV3WTLUNGLC1SQSFWT
OVARYCAOV4WTLUNGLC2ADWT
OVARYCOLO704WTLUNGLCLC103HWT
OVARYCOV318WTLUNGLCLC97TM1WT
OVARYCOV362WTLUNGLK2WT
OVARYCOV434WTLUNGLOUNH91WT
OVARYCOV504WTLUNGLU134AWT
OVARYCOV644WTLUNGLU135WT
OVARYDOV13WTLUNGLU139WT
OVARYEFO21WTLUNGLU165WT
OVARYEFO27WTLUNGLU65WT
OVARYFUOV1WTLUNGLU99WT
OVARYHS571TWTLUNGLUDLU1WT
OVARYIGROV1WTLUNGLXF289WT
OVARYJHOC5WTLUNGMERO14WT
OVARYJHOM1WTLUNGMERO25WT
OVARYJHOS2WTLUNGMERO41WT
OVARYJHOS3WTLUNGMERO48AWT
OVARYJHOS4WTLUNGMERO82WT
OVARYKGNWTLUNGMERO83WT
OVARYKURAMOCHIWTLUNGMERO84WT
OVARYMCASWTLUNGMERO95WT
OVARYNIHOVCAR3WTLUNGMORCPRWT
OVARYOAW28WTLUNGMS1WT
OVARYOAW42WTLUNGNCIH1048WT
OVARYOELEWTLUNGNCIH1092WT
OVARYONCODG1WTLUNGNCIH1105WT
OVARYOV17RWTLUNGNCIH1155WT
OVARYOV56WTLUNGNCIH1184WT
OVARYOV7WTLUNGNCIH128WT
OVARYOVCA420WTLUNGNCIH1299WT
OVARYOVCA433WTLUNGNCIH1304WT
OVARYOVCAR4WTLUNGNCIH1339WT
OVARYOVCAR5WTLUNGNCIH1341WT
OVARYOVCAR8WTLUNGNCIH1355WT
OVARYOVISEWTLUNGNCIH1373WT
OVARYOVK18WTLUNGNCIH1385WT
OVARYOVKATEWTLUNGNCIH1417WT
OVARYOVMANAWTLUNGNCIH1435WT
OVARYOVMIUWTLUNGNCIH1436WT
OVARYOVSAHOWTLUNGNCIH1437WT
OVARYOVTOKOWTLUNGNCIH146WT
OVARYPA1WTLUNGNCIH1563WT
OVARYPEO1WTLUNGNCIH1568WT
OVARYRMGIWTLUNGNCIH1573WT
OVARYRMUGSWTLUNGNCIH1581WT
OVARYSKOV3WTLUNGNCIH1618WT
OVARYSNU119WTLUNGNCIH1623WT
OVARYSNU8WTLUNGNCIH1648WT
OVARYSNU840WTLUNGNCIH1650WT
OVARYSW626WTLUNGNCIH1688WT
OVARYTOV112DWTLUNGNCIH1693WT
OVARYTOV21GWTLUNGNCIH1694WT
OVARYTYKNUWTLUNGNCIH1703WT
OVARYUWB1289WTLUNGNCIH1734WT
SKINSKMEL30D287H E275KLUNGNCIH1770WT
SKINGRMI326VLUNGNCIH1781WT
SKINHKA1I326VLUNGNCIH1792WT
SKINMM127G464E E451KLUNGNCIH1793WT
SKINHMVIIG469VLUNGNCIH1819WT
SKINHS936TN581KLUNGNCIH1836WT
SKIN451LUV600ELUNGNCIH1838WT
SKINA101DV600ELUNGNCIH1869WT
SKINA2058V600ELUNGNCIH187WT
SKINA375V600ELUNGNCIH1876WT
SKINC32V600ELUNGNCIH1915WT
SKINCOLO679V600ELUNGNCIH1930WT
SKINCOLO741V600ELUNGNCIH1944WT
SKINCOLO783V600ELUNGNCIH196WT
SKINCOLO794V600ELUNGNCIH1963WT
SKINCOLO800V600ELUNGNCIH1975WT
SKINCOLO818V600ELUNGNCIH1993WT
SKINCOLO829V600ELUNGNCIH2009WT
SKINCP50MELBV600ELUNGNCIH2023WT
SKINCP67MELV600ELUNGNCIH2029WT
SKING361V600ELUNGNCIH2030WT
SKINHMY1V600ELUNGNCIH2066WT
SKINHS294TV600ELUNGNCIH2073WT
SKINHS695TV600ELUNGNCIH2077WT
SKINHS939TV600ELUNGNCIH2081WT
SKINHT144V600ELUNGNCIH2085WT
SKINIGR37V600ELUNGNCIH209WT
SKINIGR39V600ELUNGNCIH2106WT
SKINISTMEL1V600ELUNGNCIH211WT
SKINK029AXV600ELUNGNCIH2110WT
SKINK2V600ELUNGNCIH2122WT
SKINM00921V600ELUNGNCIH2126WT
SKINM1203273V600ELUNGNCIH2135WT
SKINM14V600ELUNGNCIH2141WT
SKINM980513V600ELUNGNCIH2170WT
SKINMALME3MV600ELUNGNCIH2171WT
SKINMDAMB435SV600ELUNGNCIH2172WT
SKINMELHOV600ELUNGNCIH2196WT
SKINMM370V600ELUNGNCIH2228WT
SKINMM383V600ELUNGNCIH226WT
SKINMM386V600ELUNGNCIH2286WT
SKINMM426V600ELUNGNCIH2291WT
SKINMMACSFV600ELUNGNCIH23WT
SKINMZ7MELV600ELUNGNCIH2342WT
SKINRPMI7951V600ELUNGNCIH2347WT
SKINRVH421V600ELUNGNCIH2444WT
SKINSEKIV600ELUNGNCIH250WT
SKINSH4V600ELUNGNCIH2882WT
SKINSKMEL1V600ELUNGNCIH2887WT
SKINSKMEL24V600ELUNGNCIH292WT
SKINSKMEL28V600ELUNGNCIH3122WT
SKINSKMEL3V600ELUNGNCIH322WT
SKINSKMEL31V600ELUNGNCIH3255WT
SKINSKMEL5V600ELUNGNCIH345WT
SKINUACC257V600ELUNGNCIH358WT
SKINUACC62V600ELUNGNCIH378WT
SKINVMRCMELGV600ELUNGNCIH441WT
SKINWM1552CV600ELUNGNCIH446WT
SKINWM1799V600ELUNGNCIH460WT
SKINWM278V600ELUNGNCIH510WT
SKINWM35V600ELUNGNCIH520WT
SKINWM793V600ELUNGNCIH522WT
SKINWM88V600ELUNGNCIH524WT
SKINWM983BV600ELUNGNCIH526WT
SKINGMELV600E G759*LUNGNCIH596WT
SKINLOXIMVIV600E I208VLUNGNCIH64WT
SKINWM115V600E V600DLUNGNCIH647WT
SKINWM2664V600E V600DLUNGNCIH650WT
SKINIGR1V600E V600K V600MLUNGNCIH661WT
SKINA388WTLUNGNCIH69WT
SKINA431WTLUNGNCIH720WT
SKINCHL1WTLUNGNCIH727WT
SKINCJMWTLUNGNCIH740WT
SKINCOLO792WTLUNGNCIH748WT
SKINCP66MELWTLUNGNCIH810WT
SKINDJM1WTLUNGNCIH82WT
SKINGAKWTLUNGNCIH820WT
SKINHMCBWTLUNGNCIH835WT
SKINHS852TWTLUNGNCIH838WT
SKINHS944TWTLUNGNCIH841WT
SKINHSC1WTLUNGNCIH847WT
SKINIPC298WTLUNGNCIH889WT
SKINLB2518MELWTLUNGPC14WT
SKINLB373MELDWTLUNGPC3JPC3WT
SKINMCC13WTLUNGPC9WT
SKINMCC142WTLUNGRERFLCAD2WT
SKINMCC26WTLUNGRERFLCAIWT
SKINMELJUSOWTLUNGRERFLCFMWT
SKINMEWOWTLUNGRERFLCKJWT
SKINMM415WTLUNGRERFLCMSWT
SKINMS1WTLUNGRERFLCSQ1WT
SKINMZ2MELWTLUNGSALEWT
SKINSF8657WTLUNGSBC1WT
SKINSKMEL2WTLUNGSBC3WT
THYROID8305CV600ELUNGSBC5WT
THYROID8505CV600ELUNGSCLC21HWT
THYROIDBCPAPV600ELUNGSCLC22HWT
THYROIDBHT101V600ELUNGSHP77WT
THYROIDHTCC3V600ELUNGSKLU1WT
THYROIDIHH4V600ELUNGSKMES1WT
THYROIDK5V600ELUNGSQ1WT
THYROIDASH3WTLUNGSW1573WT
THYROIDCAL62WTLUNGSW900WT
THYROIDCGTHW1WTLUNGUMC11WT
THYROIDFTC133WTLUNGVMRCLCDWT
THYROIDFTC238WTLUNGVMRCLCPWT
THYROIDKMH2WT   
THYROIDMB1WT   
THYROIDML1WT   
THYROIDRO82W1WT   
THYROIDSW579WT   
THYROIDTTWT   
THYROIDTT2609C02WT   
  

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Citation

This paper should be referenced as such :
Domingo E
BRAF (v-raf murine sarcoma viral oncogene homolog B1)
Atlas Genet Cytogenet Oncol Haematol. 2021;25(1):23-33
Free journal version : [ pdf ]   [ DOI ]
History of this paper:
Domingo, E ; Schwartz, S Jr. BRAF (v-raf murine sarcoma viral oncogene homolog B1. Atlas Genet Cytogenet Oncol Haematol. 2004;8(4):294-298.
http://documents.irevues.inist.fr/bitstream/handle/2042/38125/09-2004-BRAFID828.pdf


Other Leukemias implicated (Data extracted from papers in the Atlas) [ 11 ]
  Diffuse red pulp small B-cell lymphoma
Disseminated Juvenile Xanthogranuloma
Early T-cell precursor acute lymphoblastic leukemia
Follicular Dendritic Cell Sarcoma
Histiocytic Sarcoma
Indeterminate Dendritic Cell Tumor
Interdigitating Dendritic Cell Sarcoma
Langerhans cell sarcoma
Langerhans cell histiocytosis
t(14;16)(q32;q23) IGH::MAF
t(5;7)(q31;q34) FCHSD1::BRAF


Other Cancer prone implicated (Data extracted from papers in the Atlas) [ 2 ]
  LEOPARD syndrome Noonan syndrome


External links

Nomenclature
HGNC (Hugo)BRAF   1097
LRG (Locus Reference Genomic)LRG_299
Cards
AtlasBRAFID828
Atlas Explorer : (Salamanque)BRAF
Entrez_Gene (NCBI)BRAF    B-Raf proto-oncogene, serine/threonine kinase
AliasesB-RAF1; B-raf; BRAF1; NS7; 
RAFB1
GeneCards (Weizmann)BRAF
Ensembl hg19 (Hinxton)ENSG00000157764 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000157764 [Gene_View]  ENSG00000157764 [Sequence]  chr7:140730665-140924929 [Contig_View]  BRAF [Vega]
ICGC DataPortalENSG00000157764
TCGA cBioPortalBRAF
AceView (NCBI)BRAF
Genatlas (Paris)BRAF
SOURCE (Princeton)BRAF
Genetics Home Reference (NIH)BRAF
Genomic and cartography
GoldenPath hg38 (UCSC)BRAF  -     chr7:140730665-140924929 -  7q34   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)BRAF  -     7q34   [Description]    (hg19-Feb_2009)
GoldenPathBRAF - 7q34 [CytoView hg19]  BRAF - 7q34 [CytoView hg38]
ImmunoBaseENSG00000157764
Genome Data Viewer NCBIBRAF [Mapview hg19]  
OMIM114500   115150   155600   163950   164757   211980   613706   613707   
Gene and transcription
Genbank (Entrez)AA252358 AA834931 AA975673 AI203435 AJ276310
RefSeq transcript (Entrez)NM_001354609 NM_001374244 NM_001374258 NM_001378467 NM_001378468 NM_001378469 NM_001378470 NM_001378471 NM_001378472 NM_001378473 NM_001378474 NM_001378475 NM_004333
Consensus coding sequences : CCDS (NCBI)BRAF
Gene ExpressionBRAF [ NCBI-GEO ]   BRAF [ EBI - ARRAY_EXPRESS ]   BRAF [ SEEK ]   BRAF [ MEM ]
Gene Expression Viewer (FireBrowse)BRAF [ Firebrowse - Broad ]
GenevisibleExpression of BRAF in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)673
GTEX Portal (Tissue expression)BRAF
Human Protein AtlasENSG00000157764-BRAF [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Conserved Domain (NCBI)BRAF
Human Protein Atlas [tissue]ENSG00000157764-BRAF [tissue]
HPRD01264
Protein Interaction databases
BioGRIDBRAF
STRING (EMBL)BRAF
ZODIACBRAF
Ontologies - Pathways
Litterature
PubMed499 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
EVEXBRAF
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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