|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for BRAF(NM_004333.5) Search again
Product ID:
HQP017733
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
B-RAF1, B-raf, BRAF-1, BRAF1, NS7, RAFB1
Gene Description:
B-Raf proto-oncogene, serine/threonine kinase
Target Gene Accession:
NM_004333.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
This gene encodes a protein belonging to the raf/mil family of serine/threonine protein kinases. This protein plays a role in regulating the MAP kinase/ERKs signaling pathway, which affects cell division, differentiation, and secretion. Mutations in this gene are associated with cardiofaciocutaneous syndrome, a disease characterized by heart defects, mental retardation and a distinctive facial appearance. Mutations in this gene have also been associated with various cancers, including non-Hodgkin lymphoma, colorectal cancer, malignant melanoma, thyroid carcinoma, non-small cell lung carcinoma, and adenocarcinoma of lung. A pseudogene, which is located on chromosome X, has been identified for this gene. [provided by RefSeq].
Gene References into function
- MEK1 interacts with B-Raf.
- somatic missense mutations in 66% of malignant melanomas and at lower frequency in a wide range of human cancers
- BRAF mutations in colorectal cancers occur only in tumours that do not carry mutations in a RAS gene known as KRAS, and BRAF mutation is linked to the proficiency of these tumours in repairing mismatched bases in DNA
- High frequency of BRAF mutations in nevi
- The V599E BRAF mutation appears to be a somatic mutation associated with melanoma development and/or progression in a proportion of affected individuals.
- results demonstrate that the mutational status of BRAF and KRAS is distinctly different among histologic types of ovarian serous carcinoma, occurring most frequently in invasive micropapillary serous carcinomas and its precursors, serous borderline tumor
- High prevalence of BRAF mutations in thyroid cancer is genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma.
- activating BRAF mutations may be an important event in the development of papillary thyroid cancer
- cAMP activates ERK and increases proliferation of autosomal dominant polycystic kindey epithelial cells through the sequential phosphorylation of PKA, B-Raf and MAPK in a pathway separate from the classical receptor tyrosine kinase cascade
- gene is mutated in skin melanoma, but not in uveal melanomas
- 13 germline BRAF variants, 4 of which were silent mutations in coding regions & 9 nucleotide substitutions in introns, were found in melanoma patients and melanoma family, but none appeared statistically likely to be a melanoma susceptibility gene.
- B-raf is involved in adhesion-independent ERK1/2 signaling in melanocytes
- Data suggest that BRAF T1796A activating mutation is not common in primary uveal melanoma.
- B-Raf has a role in extracellular signal-regulated kinase (ERK) signaling in T cells and prevents antigen-presenting cell-induced anergy
- BRAF has a role in in squamous cell carcinoma of the head and neck through uncommon mutations
- The BRAF(V599E) mutation appears to be an alternative event to RET/PTC rearrangement rather than to RAS mutations, which are rare in PTC. BRAF(V599E) may represent an alternative pathway to oncogenic MAPK activation in PTCs without RET/PTC activation.
- Mucinous ovarian cancers without a KRAS mutation have not sustained alternative activation of this signaling pathway through mutation of the BRAF oncogene.
- 3 cell lines derived from human choroidal melanoma express B-Raf containing the V599E mutation and showed a 10-fold increase in endogenous B-RafV599E kinase activity and a constitutive activation of the MEK/ERK pathway that is independent of Ras
- Mutations are not detectable in plasma cell leukemia and multiple myeloma.
- mutation of BRAF gene could be a potentially useful marker of prognosis of patients with advanced thyroid cancers
- Our findings of a high frequency of BRAF mutations at codon 599 in benign melanocytic lesions of the skin indicate that this mutation is not sufficient by itself for malignant transformation.
- Both BRAF and FBXW7 mutations functionally activate kinase effectors important in pancreatic cancer and extend potential options for therapeutic targeting of kinases in treatment of phenotypically distinct pancreatic adenocarcinoma subsets.
- BRAF mutations, which are present in a variety of other human cancers, do not seem to be involved in gastric cancer development
- Uceal melanomas arise independent of oncogenic BRAF and NRAS mutations.
- BRAF mutations were seen in stomach neoplasms.
- BRAF mutations are restricted to papillary carcinomas and poorly differentiated and anaplastic carcinomas arising from papillary carcinomas
- BRAF is occasionally mutated in NHL, and BRAF mutation may contribute to tumor development in some NHLs
- None of the cases of gastric cancer showed braf mutations
- Mutations of BRAF are associated with extensive hMLH1 promoter methylation in sporadic colorectal carcinomas
- Missense mutation is marker of colonic but not gastric cancer.
- Mutations were found in exon 15 in colorectal adenocarcinoma.
- Our data indicate that BRAF gene mutations are rare to absent events in uveal melanoma of humans.
- NRAS and BRAF mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression
- BRAF mutations are associated with proximal colon tumors with mismatch repair deficiency and MLH1 hypermethylation.
- New enriched PCR-RFLP assay for detecting mutations of BRAF codon 599 mutation in pleural mesotheliomas.
- RAS or BRAF mutations are detected in about 32% of all Barrett's adenocarcinomas; the disruption of the Raf/MEK/ERK (MAPK) kinase pathway is a frequent but also early event in the development of Barrett's adenocarcinoma
- BRAF mutations are frequently present in sporadic colorectal cancer with methylated hMLH1
- Mutations in BRAF gene is associated with malignant melanomas
- These studies identify isoprenylcysteine carboxyl methyltransferase as a potential target for reducing the growth of K-Ras- and B-Raf-induced malignancies.
- The lack or low prevalence of BRAF mutation in other thyroid neoplasms is consistent with the notion that other previously defined genetic alterations on the same signaling pathway are sufficient to cause tumorigenesis in most thyroid neoplasms.
- possible cooperation between BRAF activation and PTEN loss in melanoma development.
- mutations in the BRAF gene and to some extent in the N-ras gene represent early somatic events that occur in melanocytic nevi
- BRAF mutation may be acquired during development of metastasis but is not a significant factor for primary melanoma development and disease outcome.
- ovarian serous cystadenomas do not contain mutations in either BRAF or KRAS genes
- These results suggest that the BRAF mutation is unlikely to be involved in gastric carcinogenesis.
- BRAF(V599E) is more common genetic alteration found to date in adult sporadic papillary thyroid carcinomas (PTCs). It is unique for this thyroid cancer histotype, and it might drive the development of PTCs of classic papillary subtype.
- The finding of tandem mutations in thin melanomas makes it more likely that they arise as a simultaneous rather than sequential event.
- Radiation-induced tumors have a low prevalence of BRAF point mutations and high prevalence of RET/PTC rearrangements
- B-Raf kinase activity regulation by tuberin and Rheb is mammalian target of rapamycin (mTOR)-independent
- mucosal melanomas of the head and neck do not frequently harbor an activating mutation of BRAF
- in contrast to cutaneous melanoma, BRAF does not appear to be involved in the pathogenesis of uveal melanoma
- BRAF mutations are rather rare in solitary cold adenomas and adenomatous nodules and do not explain the molecular etiology of ras mutation-negative cold thyroid nodules.
- activation of this gene may be one of the early events in the pathogenesis of some melanomas.
- B-Raf and ERK are activated by cyclic AMP after calcium restriction
- mutated in papillary thyroid cancer.
- In this study, this BRAF mutation was demonstrated in some conjunctival melanoma tissue samples, suggesting that some conjunctival melanomas may share biological features in common with cutaneous melanoma.
- Data suggest that SPRY2, an inhibitor of ERK signaling, may be bypassed in melanoma cells either by down-regulation of its expression in WT BRAF cells, or by the presence of the BRAF mutation.
- Mutations within the BRAF gene are useful markers for the differential diagnosis between Spitz nevus and malignant melanoma.
- we found 19 cases (38%) to harbor somatic B-raf exon 15 mutations.
- Data provide evidence that B-Raf is a positive regulator of T cell receptor-mediated sustained ERK activation, which is required for NFAT activation and the full production of IL-2.
- BRAF(V599E) mutation is seven times higher in lesions with structural changes and 13 times higher in growing lesions as compared with lesions without changes
- REVIEW: our understanding of B-RAF as an oncogene and of its role in cancer
- Mutations of BRAF or KRAS oncogenes are early events in the serrated polyp neoplasia pathway. CpG island methylation plays a role in serrated polyp progression to colorectal carcinoma.
- mutated in childhood acute lymphoblastic leukemia.
- BRAF mutations are associated with conjunctival neoplasms
- AKAP9-BRAF fusion was preferentially found in radiation-induced papillary carcinomas developing after a short latency, whereas BRAF point mutations were absent in this group
- Data suggest that Rit is involved in a novel pathway of neuronal development and regeneration by coupling specific trophic factor signals to sustained activation of the B-Raf/ERK and p38 MAP kinase cascades.
- a novel Ras-independent ERK1/2 activation system in which p110gamma/Raf-1/MEK1/2 and PKA/B-Raf/MEK1/2 cooperate to activate ERK1/2.
- We found mutations in p53, K-ras, and BRAF genes in 35%, 30%, and 4% of tumors, respectively, and observed a minimal or no co-presence of these gene alterations.
- KSHV-infected cell lines expressed higher levels of B-Raf and VEGF-A; B-Raf-induced VEGF-A expression was demonstrated to be sufficient to enhance tubule formation in endothelial cells
- autoinhibition was negatively regulated by acidic substitutions at phosphorylation sites within the activation loop
- Data show that the the RET receptor (RET/PTC), Ras and BRAF function along a linear oncogenic signaling cascade in which RET/PTC induces RAS-dependent BRAF activation and RAS- and BRAF-dependent ERK activation.
- Mutations in the BRAF protooncogene (V599E)may be an alternative pathway of tumorigenesis of familial colorectal cancer.
- BRAF mutations proved to be absent in tumors from hereditary nonpolyposis colorectal cancer syndrome (HNPCC) families with germline mutations in the MMR genes MLH1 and MSH2.
- The data of this study suggest that activating mutations of B-RAF are not a frequent event in gliomas; nevertheless, when present they are associated with high-grade malignant lesions.
- B-raf mutations surrounding Thr439 found in human cancers are unlikely to contribute to increased oncogenic properties of B-raf
- These results suggest that BRAF mutations do not have a role in tumorigenesis of neuroendocrine gastroenteropancreatic tumors.
- Anaplastic thyroid carcinomas which are derived from papillary carcinomas are due to BRAF and p53 mutations
- B-raf V599E and V599K oncogenic mutations are likely to affect melanocyte-specific pathways controlling proliferation and differentiation
- The increasing frequency of BRAF mutations as a function of age could help account for the well documented but poorly understood observation that age is a relevant prognostic indicator for patients with papillary thyroid carcinoma.
- BRAF mutation occurs later in thyroid tumor progression and is restricted mainly to papillary thyroid carcinoma and anaplastic thyroid carcinoma
- Role of BRAF mutation in facilitating metastasis and progression of papillary thyroid cancer in lymph nodes.
- determination of mutation specific gene expression profiles in papillary thyroid carcinoma
- Single-cell clones with efficient knockdown of (V 600 E)B-RAF could be propagated in the presence of basic fibroblast growth factor but underwent apoptosis or senescence-like growth arrest upon withdrawal of this growth factor
- sustained BRAF(V600E) expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16(INK4a) and senescence-associated acidic beta-galactosidase (SA-beta-Gal) activity, a commonly used senescence marker
- BRAF mutation in melanoma is most likely to occur prior to the development of metastatic disease
- Although BRAF and NRAS mutations are likely to be important for the initiation and maintenance of some melanomas, other factors might be more significant for proliferation and prognosis in subgroups of aggressive melanoma
- The results showed that conjunctival nevi, similar to skin nevi, have a high frequency of oncogenic BRAF mutations.
- These data suggest that MITF is an anti-proliferation factor that is down-regulated by B-RAF signaling and that this is a crucial event for the progression of melanomas that harbor oncogenic B-RAF.
- Mutations of the BRAF gene are partly involved in the malignant transformation of the endometrium.
- selective reduction in catalytic activity and expression of B-Raf but not Raf-1 suggest that B-Raf may be playing an important role in altered ERK signaling in brain of suicide subjects, and thus in the pathophysiology of suicide
- In patients with papillary thyroid cancer, BRAF mutation is associated with poorer clinicopathological outcomes and independently predicts recurrence.
- As the BRAF oncogene is frequently found to be mutated in human cutaneous melanomas, it may constitute a risk factor for melanoma formation within CMN and DMN.
- The oncogenic B-raf mutations V599E and V599K, as early events in melanocyte transformation, persist throughout metastasis with important prognostic implications.
- copy number gain may represent another mechanism of BRAF activation in thyroid tumors
- The estimated proportion of attributable risk of melanoma due to variants in BRAF is 1.6%, but the burden of disease associated with this variant is greater than that associated with the major melanoma locus (CDKN2A) which has a risk of 0.2%.
- Mutation and elevated expression of BRAF is associated with the development of testicular germ cell tumors
- The authors have developed and run a high-throughput screen to find inhibitors of V600E BRAF using an enzyme cascade assay in which oncogenic BRAF activates MEK1, which in turn activates ERK2, which then phosphorylates the transcription factor ELK1.
- Data suggest that B-RAF activates C-RAF through a mechanism involving 14-3-3 mediated heterooligomerization and C-RAF transphosphorylation.
- V600E B-Raf requires the Hsp90 chaperone for stability and is degraded in response to Hsp90 inhibitors.
- activating mutations of PDGFR-alpha, c-kit and B-RAF are absent in gliosarcomas
- V599E BRAF mutation was uncommon in Japanese lung cancer.
- aberrant B-Raf activity in angiomyolipomas leads to abnormal cellular differentiation and migration [review]
- The most frequent B-RAF gene alterations are not involved in prostate carcinogenesis
- BRAF mutation does not seem to be sufficient to produce MAPK activation in melanocytic nevi.
- gain-of-function BRAF signaling is strongly associated with in vivo tumorigenicity
- findings demonstrate that heterogeneous de novo missense mutations in three genes within the mitogen-activated protein kinase pathway, BRAF, MEK1 and MEK2 cause cardio-facio-cutaneous syndrome
- wild-type B-Raf-mediated ERK1/2 activation plays a major role in proliferation and transformation of uveal melanocytes; Raf-1 is not involved in this activation
- NRAS and BRAF activating mutations can coexist in the same melanoma, but are mutually exclusive at the single-cell level
- Cardio-facio-cutaneous (CFC) syndrome involves dysregulation of the RAS-RAF-ERK pathway.
- Merlin and MLK3 can interact in situ and merlin can disrupt the interactions between B-Raf and Raf-1 or those between MLK3 and either B-Raf or Raf-1.
- Melanoma cells require either B-RAF or phosphoinositide-3 kinase activation for protection from anoikis.
- BRAF V600E is associated with a high risk of recurrence and less differentiated papillary thyroid carcinoma due to the impairment of Na+/I- targeting to the membrane
- UV light is not necessarily required for the acquisition of the BRAF(V600E) mutation, and non-mutagenic effects of UV light to melanocytes may be more important in the nevogenesis
- BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma
- B-RAF (V600E) was confirmed to be associated with the papillary growth pattern, but not with poorer differentiated papillary thyroid carcinoma variants.
- among 23 melanomas located at body sites with chronic UV exposure, only a single tumour harboured the B-raf V599E mutation which was a significantly lower frequency in comparison to melanomas from sun-protected body sites
- a BRAFT1799A mutation may have a role in poor differentiation of thyroid carcinoma
- A subset of Spitz nevi, some with atypical histologic features, possess BRAF mutations. The BRAF mutational status does not separate all Spitz nevi from spitzoid melanomas and non-Spitz types of melanocytic proliferations, contrary to previous reports.
- Rheb has a central role in the regulation of the Ras/B-Raf/C-Raf/MEK signaling network
- CpG island methylator phenotype-positive colorectal tumors represent a distinct subset, encompassing almost all cases of tumors with BRAF mutation
- findings show that MC1R variants are strongly associated with BRAF mutations in non-chronic sun-induced damage melanomas; in this subtype, risk for melanoma associated with MC1R is due to increase in risk of developing melanomas with BRAF mutations
- BRAF mutation is associated with melanoma and melanocytic nevi.
- Thus, we propose that the hitherto unidentified function of the B-Raf amino-terminal region is to mediate calcium-dependent activation of B-Raf and the following MEK activation, which may occur in the absence of Ras activation.
- Aberrant methylation and hence silencing of TIMP3, SLC5A8, DAPK and RARbeta2, in association with BRAF mutation, may be an important step in PTC tumorigenesis and progression.
- BRAF mutation was frequent in hyperplastic polyps (67%) and sessile serrated adenomas (81%).
- B-RAF has been identified as the most mutated gene in invasive cells and therefore an attractive therapeutic target in melanoma.
- BRAF mutations are associated with colorectal cancers
- Expression of p27Kip1 in melanoma is regulated by B-RAF at the mRNA level and via B-RAF control of Cks1/Skp2-mediated proteolysis.
- Single nucleotide polymorphism found exclusively in papillary thyroid carcinoma.
- BRAF, K-ras and BAT26 are expressed in colorectal polyps and stool
- BRAF, K-ras and BAT26 are expressed in colorectal polyps and stool [BAT26]
- Braf mutations in thyroid tumorigenesis.
- Concomitant KRAS and BRAF mutations increased along progression of MSS colorectal cancer, suggesting that activation of both genes is likely to harbour a synergistic effect
- BRAFV600E activates not only MAPK but also NF-kappaB signaling pathway in human thyroid cancer cells, leading to an acquisition of apoptotic resistance and promotion of invasion.
- Extracellular signal-regulated kinase-3 (ERK3/MAPK6) is highly expressed in response to BRAF signaling.
- BRAF T1976A mutation is present at high frequency in benign naevi such as Spitz and Reed.
- data support a model in which mutational activation of BRAF in human melanomas contributes to constitutive induction of NF-kappaB activity and to increased survival of melanoma cells
- Normally, BRAF alone is responsible for signaling to MEK. However, when RAS is mutated in melanoma, melanocytes switch their signaling from BRAF to CRAF.
- Activating BRAF mutation is associated with papillary thyroid carcinoma
- BRAF mutation remained a significant prognostic factor for lymph node metastasis (odds ratio = 10.8, 95% confidence interval, 3.5-34.0, P < 0.0001).
- phosphorylation on both S365 and S429 participate in the differential regulation of B-Raf isoforms through distinct mechanisms
- data provide evidence that oncogenic properties of BRAF contribute to the tumorigenesis of intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC), but at a lower frequency than KRAS
- BRAF-V600E mutations are mainly involved in colorectal cancer families characterized by an increased risk of other common malignancies
- Association with preexisting nevi and pronounced infiltration of lymphocytes was significantly higher in BRAF mutated melanoma tumours
- Previously identified associations between smoking and colon cancer, whether microsatellite unstable or stable, appear to be explained by the association of smoking with BRAF mutation.
- BRAF(T1799A) mutation is associated with a lower rate of tumor proliferation.
- RASSF1A methylation was observed in a high frequency in endometrioid endometrial carcinoma whereas K-ras and B-raf mutations were observed in a low frequency
- The role for BRAF activation in thyroid cancer development and establishing the potential therapeutic efficacy of BRAF-targeted agents in patients with thyroid cancerwill be reviewed.
- BRAF mutation is associated with thyroid carcinogenesis
- there is a subgroup of colorectal carcinomas which develop via the microsatellite instability pathway that carry an alteration of the BRAF gene
- Absence of association between BRAF mutation and activation of MAPK pathway in papillary thyroid carcinoma suggests the presence of mechanisms that downregulate MAPK activation.
- Copy gain of PDGFB occurs in a subset of tumors showing no evidence of mutated BRAF or rearranged ret, suggesting that copy gain of PDGFB may underlie the increased expression of platelet-derived growth factor described recently in the literature.
- characterization of the T1799-1801del and A1799-1816ins BRAF mutations in papillary thyroid cancer; the two new mutations resulted in constitutive activation of the BRAF kinase and caused NIH3T3 cell transformation
- Overexpression of B-Raf mRNA and protein may be a feature of nonfunctioning pituitary adenomas, highlighting overactivity of the Ras-B-Raf-MAP kinase pathway in these tumors.
- BRAF gene plays a "gatekeeper" role but does not act as a predisposition gene in the development of low-grade ovarian serous carcinomas
- BRAFV600E represents a detectable marker in the plasma/serum from melanoma patients for monitoring but not diagnostic purposes
- B-RAF mutations are a rare event in pituitary tumorigenesis.
- The aim of this study was to identify the effect that BRAF oncogene has on post-transcriptional regulation in papillary thyroid carcinoma by using microRNA analysis.
- findings show that RASSF1A hypermethylation and KRAS mutations and BRAF mutations are inversely correlated and play an important role in the development of cervical adenocarcinomas
- mutational analysis of KRAS, BRAF, and MAP2K1/2 in 56 patients with CFC syndrome; comparison of the genotype-phenotype correlation of CFC with that of Costello syndrome suggest a significant clinical overlap but not genotype overlap.
- BRAF(V600E) mutation is identified in a subset of cutaneous metastases from papillary thyroid carcinomas
- data suggest that BRAF mutations might be present less frequently than KRAS mutations in Greek patients with colorectal carcinomas
- finding of a strong association between BRAF mutations and serrated histology in hyperplastic aberrant crypt foci supports the idea that these lesions are an early, sentinel, or a potentially initiating step on the serrated pathway to colorectal carcinom
- BRAF V600E mutation was occasionally observed in anaplastic carcinomas with papillary carcinoma.
- MSI is rare in UC-related neoplasia as well as non-neoplastic lesions, and does not contribute to the development of dysplasia.
- prevalence of BRAF mutation and RET/PTC were determined in diffuse sclerosing variant of papillary thyroid carcinoma; none of the cases showed a BRAF mutation
- Molecular diagnosis and careful observations should be considered in children with Cardio-facio-cutaneous syndrome because they have germline mutations in BRAF and might develop malignancy.
- c-kit expression is not alternative to BRAF and/or KRAS activation.
- BRAF V600E mutation in PTCs is associated with reduced expression of key genes involved in iodine metabolism
- data indicate that both early-life UV exposure and nevus propensity contribute to occurrence of BRAF+ melanoma, whereas nevus propensity and later-life sun exposure influence the occurrence of NRAS+ melanoma
- analysis of a BRAF mutation-associated gene expression signature in melanoma
- low rate of RAS-RAF mutations (2/22, 9.1%) observed in Spitz melanocytic nevi suggests that these lesions harbor as yet undetected activating mutations in other components of the RAS-RAF-MEK-ERK-MAPK pathway
- frequency of the BRAF mutation and the associations between BRAF mutation and clinicopathologic parameters in papillary thyroid carcinoma were evaluated by meta-analysis
- T1790A BRAF mutation (L597Q) in childhood acute lymphoblastic leukemia is a functional oncogene
- The heterogeneous distribution of BRAF mutations suggests that discrete tumor foci in multifocal PTC may occur as independent tumors.
- Presence of BRAF V600E in very early stages of papillary thyroid carcinoma.
- influence of B-RAF-specific RNA interference on the proliferation and apoptosis of gastric cancer BGC823 cell line
- We conclude that screening for BRAF 15 exon mutation is an efficient tool in the diagnostic strategy for HNPCC
- In contrast to C-RAF that requires farnesylated H-Ras, cytosolic B-RAF associates effectively and with significantly higher affinity with both farnesylated and nonfarnesylated H-Ras.
- KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not
- PPARbeta/delta has a role in growth of RAF-induced lung adenomas
- BRAF V600E mutation in papillary carcinoma of the thyroid may facilitate tumor cell growth and progression once seeded in the lymph nodes.
- There was no coexistence of BRAF (V600E) mutation in papillary thyroid carcinoma.
- data showed differences in gene expression between nevi with and without the V600E BRAF mutation. Moreover, nevi with mutations showed over-expression of genes involved in melanocytic senescence and cell cycle inhibition
- RNA interference and pharmacologic approaches were used to assess the role of B-Raf activation in the growth of human melanomas and additionally determined if a similar role for mutant B-Raf is seen for colorectal carcinoma cell lines.
- 5 unreported mutations (T241P, Q262R, G464R, E501V, N581K) were found in cardio-facio-cutaneous syndrome. A hotspot in exon 6 at Q257 was found.
- diffuse expression of wild-type and/or mutant B-Raf may be involved in the tumorigenic process
- BRAF V600E mutation is primarily present in conventional papillary thyroid cancer; it is associated with an aggressive tumor phenotype and higher risk of recurrent and persistent disease in patients with conventional papillary thyroid cancer
- Develompment of malignant strumo ovarii with papillary thyroid carcinoma features is associated with BRAF mutations.
- BRAF(V600E) mutation detected on fine-needle aspiration biopsy specimens, more than RET/PTC rearrangements, is highly specific for papillary thyroid carcinoma.
- BRAF V600E mutation is associated with high-risk papillary thyroid carcinoma
- BRAFV600E mutations were found in 41.2% of the papillary thyroid carcinomas
- MEK inhibition is cytostatic in papillary thyroid cancer and anaplastic thyroid cancer cells bearing a BRAF mutation
- effects of a MEK inhibitor, CI-1040, on thyroid cancer cells, some of which, particularly cell proliferation and tumor growth, seemed to be BRAF mutation or RAS mutation selective
- BRAF mutation is associated as early as the hyperplastic polyp stage followed by microsatellite instability at the carcinoma stage
- Examined associations between BRAF mutations, morphology, and apoptosis in early colorectal cancer.
- BRAF mutation represents a novel indicator of the progression and aggressiveness of papillary thyroid cancer (Review)
- BRAF interacts with PLCepsilon1 in nephrotic syndrome type 3. Both proteins are coexpressed and colocalize in developing and mature glomerular podocytes.
- In this small study, the T1799A BRAF mutation was identified in almost half of the iris melanoma tissues samples examined. This finding suggests that there may be genetic as well as clinical differences between iris and posterior uveal melanomas.
- These results suggest that papillary thyroid carcinomas with BRAF (V600E) mutation are more aggressive than those with wildtype BRAF.
- mutation of N-RAS or B-RAF, signature genetic lesions present in most MMs, potently induced the expression of cell-surface CD200, a repressor of DC function.
- no BRAF mutations identified in 65 screened JMML patients; this gene is unlikely to play a role in the pathogenesis of JMML.
- The BRAF mutation is common in melanomas, but variation in rates across melanoma subtypes points to a complex interplay between BRAF activation and other factors (eg, sun exposure).
- the results of HRAS, BRAF and MAP2K1/2 mutation screening in a large cohort of patients with CS and CFC
- Detection of BRAF improves the diagnosis in fine-needle biopsy with cytological findings suspicious for papillary thyroid carcinoma.
- BRAF and MEK1/2 mutations may be more common than anticipated in ovarian cancer which could have important implications for treatment of patients with this disease and suggests potential new therapeutic avenues
- B-Raf(V600E) signaling deregulates the mitotic spindle checkpoint through stabilizing Mps1 levels in melanoma cells.
- BRAF provides proliferation and survival signals in MSI colorectal carcinoma cells displaying BRAF(V600E) but not KRAS mutations.
- Because of the very sensitive pyrophosphorolysis-activated polymerization (PAP)technology, B-RAF mutations were found in cell lines and primary uveal melanomas.
- A worse clinical outcome was found for CIMP-high, microsatellite stable colorectal cancer with KRAS/BRAF mutation but not for those lacking KRAS/BRAF mutation.
- frequency of the occurrence of BRAF mutation and/or RET/PTC in H4-PTEN positive tumors was extremely high (75%) in papillary thyroid carcinoma
- BRAF mutation is not associated with cutaneous melanoma
- Important signalling role in T cell development.
- Follicular histotypes of oncocytic thyroid carcinomas do not carry BRAF mutations
- Mutant B-RAF mediates resistance to anoikis via Bad and Bim.
- A genome-wide RNA-interference screening to identify genes required for an activated BRAF oncogene to block proliferation of fibroblasts and melanocytes revealed that a IGFBP7, has a central role in BRAF-mediated senescence and apoptosis.
- BRAF T1799A mutation is associated with aggressive pathological outcomes of papillary thyroid cancer
- BRAF(V600E) mutation is asscoiated with papillary thyroid cancer
- BRAF-V600E mutation is associated with familial non-medullary thyroid carcinoma
- Mitogen-activated protein kinase (MAPK) activity is subject to regulation even in BRAF/NRAS mutant melanoma cells and that high MAPK pathway signaling may be important only in distinct subsets of tumor cells.
- RKIP could play an important role in the down-regulation of wild-type BRAF, serving thus as an endogenous inhibitor of the MAPK pathway in nasal polyps and their adjacent turbinate mucosa.
- BRAF mutation testing of papillary thyroid carcinoma might improve the diagnosis, prognostic stratification and treatment of these tumors.
- This study confirms that the known MC1R-melanoma risk association is confined to subjects whose melanomas harbor BRAF mutations.
- BRAF mutation is associated with disease stabilization in melanoma
- Thyroid cancers with BRAF mutation are preferentially sensitive to MEK inhibitors.
- Detecting BRAF mutation by pyrosequencing is more sensitive, faster, and less expensive than direct DNA sequencing.
- K-RAS and BRAF mutations are a frequent genetic event in our samples of sporadic papillary and medullary thyroid carcinoma.
- is commonly activated by somatic point mutation, it may provide possible diagnostic and therapeutic targets in human malignant tumors.
- Results implicate aberrant activation of the MAPK pathway due to gene duplication or mutation of BRAF as a molecular mechanism of pathogenesis in low-grade astrocytomas and suggest inhibition of the MAPK pathway as a potential treatment.
- Aberrant BRAF and INK4A functionally interact to promote growth and survival of melanoma cells.
- in melanocytic lesions, BRAF(V600E) mutation can affect a subset of the cells and is associated with the type and quantity of sun exposure
- study describes the biochemical characterization of novel BRAF and MEK germline mutations in cardio-facio-cutaneous syndrome
- CpG island methylator phenotype in colorectal neoplasms may result from activating mutations in either BRAF or KRAS.
- Akt3 and mutant V600E B-Raf cooperate to promote early melanoma development.
- oncogenic BRAF inhibition can have a different effect on cell fate depending on the cellular type
- aberrant methylation of the hMLH1 gene may play a role in BRAF mutation-promoted thyroid tumorigenesis
- study revealed a significant correlation of BRAFV600E mutation with a lower expression of both sodium iodide symporter and thyroperoxidase in papillary thyroid cancer
- Shorter overall survival in primary melanoma was associated with the presence of ulceration and BRAF exon 15 mutations, as well as the absence of nuclear activation of Akt and of cytoplasmic activation of ERK.
- BRAF mutations in colorectal cancer microsatellite-stable cases are associated with high levels of chromosomal instability that are likely responsible for the adverse outcomes in these cases
- a significant relationship in overall survival in colon cancer patients with defective DNA mismatch repair and the presence of a specific mutation in BRAF (V600E)
- Compared to melanomas without BRAF mutations, melanomas with BRAF mutations showed statistically significantly higher degrees of intraepidermal scatter of melanocytes, and a higher proportion of melanocytes arranged in nests.
- Rac1b and B-Raf(V600E) functionally cooperate to sustain colorectal cell viability and suggest they constitute an alternative survival pathway to oncogenic K-Ras
- V600E BRAF mutation is associated with imatinib-resistant gastrointestinal stromal tumors
- MLH1 methylation and BRAF mutations are associated with microsatellite unstable colon tumors
- The frequencies of LOHs of 17q21, 17p13, 10q23, and 22q13 were higher in tumors with lymph node metastasis, suggesting that these LOHs may be important in increased lymph node metastasis.
- People of southern European origin had lower risk of colorectal cancers with CIMP and BRAF mutation than people of Anglo-Celtic origin, which may in part be due to genetic factors that are less common in people of southern European origin.
- BRAF regulates melanoma proliferation through the lineage specific factor MITF
- co-overexpression of KIT/CDK4 is a potential mechanism of oncogenic transformation in some BRAF/NRAS wild-type melanomas
- lung adenocarcinoma of mixed type with a high incidence of papillary and lepidic growth may be worthwhile investigating for BRAF-V600E mutation as more genetically oriented drug therapies emerge.
- hyperactivation of the MAPK pathway following activation of an inducible form of oncogenic C-Raf induces a senescence-like proliferation arrest in B-Raf mutant melanoma cells
- N-RAS(Q61K) and B-RAF(V600E) contribute to melanoma's resistance to apoptosis in part by downregulating Bim expression
- CST6, CXCL14, DHRS3, and SPP1 are regulated by BRAF signaling and may play a role in papillary thyroid carcinoma pathogenesis
- The BRAF(V600E) mutation was demonstrated to be a poor prognostic factor independent from other clinicopathological features.
- Identification and functional characterization of a novel T599I-VKSR(600-603)del BRAF mutation in a patient with follicular variant papillary thyroid carcinoma.
- These data suggest that regulation of BIM expression by BRAF-->MEK-->ERK signaling is one mechanism by which oncogenic BRAF(V600E) can influence the aberrant physiology of melanoma cells.
- focal gains at chromosome 7q34 and increased BRAF-MEK-ERK signaling are common findings in sporadic pilocytic astrocytomas
- presence of the BRAF (V600E) mutation,the incidence of microsatellite instability high colorectal cancer in populations based study.
- KRAS and BRAF mutations can impair response to anti-EGFR therapy for colorectal neoplasms
- BRAF mutation is associated with the CpG island methylator phenotype in colorectal cancer from young patients
- BRAF, KRAS and PIK3CA mutations occur prior to malignant transformation demonstrating that these oncogenic alterations are primary genetic events in colorectal carcinogenesis
- These data implicates a mitotic role for B-Raf in regulating spindle formation and the spindle checkpoint in human somatic cells.
- study identified a group of melanomas with low-activity BRAF mutations (G469E- and D594G) that are reliant upon CRAF-mediated survival activity
- BRAF mutation occurs independently of CpG island methylator phenotype and MSI in all types of serrated polyps and may serve as a marker of serrated pathway of colorectal carcinogenesis
- study concludes a single endogenous BRAF(V600E) allele is sufficient to repress BIM & prevent death from growth factor withdrawal; colorectal cancer cells with V600E mutations are addicted to the ERK1/2 pathway for repression of BIM
- CIMP-high appears to be an independent predictor of a low colon cancer-specific mortality, while BRAF mutation is associated with a high colon cancer-specific mortality.
- With at least 3 markers methylated, new CIMP-positive colorectal cancers were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation.
- Hereditary pancreatitis patients with PRSS1 mutations also had mutations in BRAF and KRAS2.
- study shows high expression of p16(INK4a) or the absence of activated B-RAF correlates with in vivo response of melanoma to cytotoxic drugs
- rearrangement, which was not observed in a series of 244 higher-grade astrocytomas, results in an in-frame fusion gene incorporating the kinase domain of the BRAF oncogene
- the T1799A BRAF mutation is present in a proportion of posterior uveal melanomas but within these tumours the distribution of the mutation is heterogeneous.
- 8% of sporadic colorectal tumors in this study harbor mutation in the BRAF gene.
- Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.
- BRAF-V600E mutation is uncommon in endocrine tumors other than thyroid papillary carcinomas
- ovarian cancer patients with KRAS or BRAF mutations may benefit from CI-1040 treatment
- Genetic extinction of BRAF(V600E) in established prostate tumors did not lead to tumor regression, indicating that while sufficient to initiate development of invasive prostate adenocarcinoma, BRAF(V600E) is not required for its maintenance.
- BRAF pseudogene activation may play a role in thyroid tumor development.