gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 29 Mar 2014.

V-raf murine sarcoma viral oncogene homolog B1

BRAF
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, Jul 2008] (from NCBI)
Top mentioned proteins: Raf, KRAS, CAN, HAD, EGFR
Papers using BRAF antibodies
Induction of autophagy and inhibition of melanoma growth in vitro and in vivo by hyperactivation of oncogenic BRAF
Supplier
Pal Soumitro, In PLoS ONE, 2009
... All primary antibodies were purchased from Cell Signaling Technology except the following: anti-BRAF from Santa Cruz Biotechnology, anti-CRAF from BD Biosciences, ...
RET/PTC rearrangements in thyroid nodules: studies in irradiated and not irradiated, malignant and benign thyroid lesions in children and adults
Supplier
LiVolsi Virginia A et al., In CytoJournal, 2000
... The amplified products were electrophoresed on a 1.2% gel at 110 V for 1.5 hours and the BRAF bands (~220 bp) were cut using sterile blade and purified using Qiagen Gel Extraction Kit (Hilden, ...
A specific inhibitor of phosphatidylinositol 3-kinase, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002)
Supplier
Brinker Achim et al., In Current Chemical Genomics, 1993
... Unconjugated B-Raf antibody was from Santa Cruz Biotechnology (sc-5284), pMEK1/2 antibody from ...
Papers on BRAF
DNA methylation subgroups and the CpG island methylator phenotype in gastric cancer: a comprehensive profiling approach.
New
Soong et al., In Bmc Gastroenterol, 28 Apr 2014
Methylation data was analysed using a recursively partitioned mixture model and investigated for associations with clinicopathological and molecular features including age, Helicobacter pylori status, tumor site, patient survival, microsatellite instability and BRAF and KRAS mutations.
Disruption of mutated BRAF signaling modulates thyroid cancer phenotype.
New
Tiwari et al., In Bmc Res Notes, 28 Apr 2014
Our laboratory evaluated cellular phenotypic effects in response to treatment with PLX4032, a BRAFV600E-specific inhibitor, in normal BRAF-wild-type thyroid cells and in BRAFV600E-positive papillary thyroid cancer cells.
BRAF V600E mutational status in pediatric thyroid cancer.
New
Grigsby et al., Saint Louis, United States. In Pediatr Blood Cancer, 27 Apr 2014
There is no clear explanation of this difference although previous studies have demonstrated a lower prevalence of the BRAF(V600E) mutation in PTC of children.
Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma.
New
Impact
Bernards et al., Amsterdam, Netherlands. In Nature, 26 Apr 2014
UNLABELLED: Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably.
Highly potent and selective 3-N-methylquinazoline-4(3H)-one based inhibitors of B-Raf(V600E) kinase.
New
Rudolph et al., Boulder, United States. In Bioorg Med Chem Lett, 13 Apr 2014
UNLABELLED: Herein we describe the design of a novel series of ATP competitive B-Raf inhibitors via structure-based methods.
Inhibition of CRM1-dependent nuclear export sensitizes malignant cells to cytotoxic and targeted agents.
Review
New
Sullivan et al., Tampa, United States. In Semin Cancer Biol, 11 Apr 2014
Potential combinatorial therapies discussed include the use of CRM1 inhibitors and the addition of alkylating agents (melphalan), anthracyclines (doxorubicin and daunomycin), BRAF inhibitors, platinum drugs (cisplatin and oxaliplatin), proteosome inhibitors (bortezomib and carfilzomib), or tyrosine-kinase inhibitors (imatinib).
Incidence of New Primary Melanomas After Diagnosis of Stage III and IV Melanoma.
New
Impact
Long et al., Essen, Germany. In J Clin Oncol, 10 Apr 2014
PURPOSE: New primary melanomas (NPMs) have developed in some patients with metastatic melanoma treated with BRAF inhibitors.
Changes in Colorectal Carcinoma Genomes under Anti-EGFR Therapy Identified by Whole-Genome Plasma DNA Sequencing.
New
Speicher et al., Graz, Austria. In Plos Genet, 31 Mar 2014
Here we analyzed plasma DNA from ten patients treated with anti-EGFR therapy by whole genome sequencing (plasma-Seq) and ultra-sensitive deep sequencing of genes associated with resistance to anti-EGFR treatment such as KRAS, BRAF, PIK3CA, and EGFR.
Broad-Spectrum Therapeutic Suppression of Metastatic Melanoma through Nuclear Hormone Receptor Activation.
New
Impact
Tavazoie et al., New York City, United States. In Cell, 27 Mar 2014
Importantly, LXRβ activation displayed melanoma-suppressive cooperativity with the frontline regimens dacarbazine, B-Raf inhibition, and the anti-CTLA-4 antibody and robustly inhibited melanomas that had acquired resistance to B-Raf inhibition or dacarbazine.
Vemurafenib in patients with BRAF(V600) mutated metastatic melanoma: an open-label, multicentre, safety study.
New
Impact
Blank et al., Milano, Italy. In Lancet Oncol, 26 Mar 2014
BACKGROUND: The orally available BRAF kinase inhibitor vemurafenib, compared with dacarbazine, shows improved response rates, progression-free survival (PFS), and overall survival in patients with metastatic melanoma that has a BRAF(V600) mutation.
[Therapeutic impact of molecular diagnosis in metastatic non-small cell lung cancer: Targeted therapies in 2013.]
Review
New
Fabre et al., Paris, France. In Rev Pneumol Clin, 22 Mar 2014
Finally, we will describe more recently known molecular alterations such as ROS1 or RET rearrangements and HER2, BRAF, PIK3CA, DDR2 mutations.
[Molecular profiling of non-small cell lung cancer.]
Review
New
Blons et al., Paris, France. In Rev Pneumol Clin, 21 Mar 2014
Since then, multiple genetic alterations (KRAS, HER2, BRAF, PIK3CA, ALK, ROS, RET…) have been identified as potential target of novel therapies, and molecular profiling has become common practice.
Pilocytic astrocytoma: a review of genetic and molecular factors, diagnostic and prognostic markers.
Review
New
Jozwiak et al., Warsaw, Poland. In Histol Histopathol, 20 Mar 2014
Nevertheless, the most important causative factors seem to be NF1 gene inactivation, in cases related to neurofibromatosis type 1, and BRAF gene overexpression in sporadic PAs, both resulting in MAPK/Erk pathway upregulation.
The scope of nanoparticle therapies for future metastatic melanoma treatment.
Review
New
Impact
Sherwood et al., Norwich, United Kingdom. In Lancet Oncol, Jan 2014
Some of the most promising therapies that have been developed include ipilimumab, an anti-cytotoxic T lymphocyte antigen 4 antibody that enhances T-cell activity in the tumour, and selective BRAF inhibitors, such as vemurafenib that blocks tumour cell proliferation in patients with activating BRAF mutations.
Targeted therapies in development for non-small cell lung cancer.
Review
Dy et al., Bangkok, Thailand. In J Carcinog, 2012
In non-small cell lung cancer (NSCLC), the ErbB family of receptors (e.g., EGFR [epidermal growth factor receptor], HER2 [human epidermal growth factor receptor 2]), RAS (rat sarcoma gene), BRAF (v-raf murine sarcoma viral oncogene homolog B1), MAPK (mitogen-activated protein kinase) c-MET (c-mesenchymal-epithelial transition), FGFR (fibroblast growth factor receptor), DDR2 (discoidin domain receptor 2), PIK3CA (phosphatidylinositol-4,5-bisphosphate3-kinase, catalytic subunit alpha)), PTEN (phosphatase and tensin homolog), AKT (protein kinase B), ALK (anaplastic lym phoma kinase), RET (rearranged during transfection), ROS1 (reactive oxygen species 1) and EPH (erythropoietin-producing hepatoma) are key targets of various agents currently in clinical development.
The intermediate-activity (L597V)BRAF mutant acts as an epistatic modifier of oncogenic RAS by enhancing signaling through the RAF/MEK/ERK pathway.
GeneRIF
Pritchard et al., Leicester, United Kingdom. In Genes Dev, 2012
endogenous expression of (L597V)Braf leads to approximately twofold elevated Braf kinase activity and weak activation of the Mek/Erk pathway
BRAF duplications and MAPK pathway activation are frequent in gliomas of the optic nerve proper.
GeneRIF
Eberhart et al., Baltimore, United States. In J Neuropathol Exp Neurol, 2012
The results of this study supported an important role for BRAF duplication and MAPK pathway activation in gliomas of the optic nerve proper.
BRAF mutation in papillary thyroid cancer and its value in tailoring initial treatment: a systematic review and meta-analysis.
Review
GeneRIF
Xing et al., Baltimore, United States. In Medicine (baltimore), 2012
Thus, in this meta-analysis, the BRAF mutation in PTC was significantly associated with PTC recurrence, lymph node metastasis, extrathyroidal extension, and advanced stage AJCC III/IV.
KRAS and BRAF mutations in Serbian patients with colorectal cancer.
GeneRIF
Jankovic et al., Belgrade, Serbia. In J Buon, 2012
the spectrum and frequency distribution of the identified KRAS and BRAF mutations in Serbian patient with colorectal cancer are in good accordance with literature data.
A cardio-facio-cutaneous syndrome case with tight Achilles tendons.
GeneRIF
Ozkinay et al., İzmir, Turkey. In Genet Couns, 2011
Cardio-facio-cutaneous syndrome is caused by heterogeneous mutations in BRAF gene.
share on facebooktweetadd +1mail to friends