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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Jul 2015.

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: KRAS, CAN, Raf, 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
Clinicopathologic features associated with efficacy and long-term survival in metastatic melanoma patients treated with BRAF or combined BRAF and MEK inhibitors.
New
Long et al., Sydney, Australia. In Cancer, 28 Aug 2015
METHODS: For 142 consecutive immunotherapy- and MAPK inhibitor-naive patients with BRAF-mutant metastatic melanoma who were treated during clinical trials with BRAF inhibitors (n = 111) or a combination of dabrafenib and trametinib (n = 31), clinicopathologic factors were correlated with the response to MAPK inhibitors and survival.
Exome sequencing identifies recurrent mutations in NF1 and RASopathy genes in sun-exposed melanomas.
New
Impact
Halaban et al., New Haven, United States. In Nat Genet, 27 Aug 2015
Our analysis established NF1, encoding a negative regulator of RAS, as the third most frequently mutated gene in melanoma, after BRAF and NRAS.
Genetics and Genetic Biomarkers in Sporadic Colorectal Cancer.
New
Jung et al., Ann Arbor, United States. In Gastroenterology, 24 Aug 2015
Commonly observed alterations across sporadic CRCs have allowed classification into a: (1) hypermutated group that includes defective DNA mismatch repair with microsatellite instability (MSI) and POLE mutations in ∼15%, containing multiple frameshifted genes and BRAF(V600E); (2) non-hypermutated group with multiple somatic copy number alterations and aneuploidy in ∼85%, containing oncogenic activation of KRAS and PIK3CA and mutation and loss of heterozygosity of tumor suppressor genes such as APC and TP53; (3) CpG Island Methylator Phenotype CRCs in ∼20% that overlap greatly with MSI CRCs and some non-hypermutated CRCs; and (4) elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) in ∼60% that associates with metastatic behavior in both hypermutated and non-hypermutated groups.
Analysis of circulating DNA and protein biomarkers to predict the clinical activity of regorafenib and assess prognosis in patients with metastatic colorectal cancer: a retrospective, exploratory analysis of the CORRECT trial.
New
Impact
Van Cutsem et al., Barcelona, Spain. In Lancet Oncol, 13 Aug 2015
METHODS: We used BEAMing technology to identify KRAS, PIK3CA, and BRAF mutations in DNA obtained from the plasma of 503 patients with metastatic colorectal cancer who enrolled in the CORRECT trial.
A Synergistic Interaction between Chk1- and MK2 Inhibitors in KRAS-Mutant Cancer.
New
Impact
Reinhardt et al., Köln, Germany. In Cell, 02 Aug 2015
Here, we perform a cell-line-based screen and identify strong synergistic interactions between cell-cycle checkpoint-abrogating Chk1- and MK2 inhibitors, specifically in KRAS- and BRAF-driven cells.
Pembrolizumab versus investigator-choice chemotherapy for ipilimumab-refractory melanoma (KEYNOTE-002): a randomised, controlled, phase 2 trial.
New
Impact
Daud et al., Los Angeles, United States. In Lancet Oncol, 23 Jul 2015
BACKGROUND: Patients with melanoma that progresses on ipilimumab and, if BRAF(V600) mutant-positive, a BRAF or MEK inhibitor or both, have few treatment options.
Genomic Classification of Cutaneous Melanoma.
New
Impact
Cancer Genome Atlas Network et al., In Cell, 18 Jul 2015
We establish a framework for genomic classification into one of four subtypes based on the pattern of the most prevalent significantly mutated genes: mutant BRAF, mutant RAS, mutant NF1, and Triple-WT (wild-type).
Gaining momentum: New options and opportunities for the treatment of advanced melanoma.
Review
New
Hoeller et al., Lausanne, Switzerland. In Cancer Treat Rev, 04 Jul 2015
A greater understanding of the epidemiology and biology of disease has underpinned the development of newer therapies, including six agents that have been approved in the EU, US and/or Japan: a cytotoxic T-lymphocyte antigen-4 inhibitor (ipilimumab), two programmed cell death-1 receptor inhibitors (nivolumab and pembrolizumab), two BRAF inhibitors (vemurafenib and dabrafenib) and a MEK inhibitor (trametinib).
[DNA mismatch repair and BRAF status in colorectal cancer: Interest for the therapeutic management?].
Review
New
André et al., Paris, France. In Bull Cancer, 30 Jun 2015
CMS1 is enriched for CRC with deficient DNA mismatch repair system (dMMR) and tumors with mutated BRAF.
Novel Approaches to Treatment of Advanced Melanoma: A Review on Targeted Therapy and Immunotherapy.
Review
New
Czajkowski et al., Bydgoszcz, Poland. In Biomed Res Int, Dec 2014
From 2011 until now, the U.S. FDA has approved seven novel agents, such as BRAF-inhibitors (vemurafenib 2011, dabrafenib 2013), MEK-inhibitors (trametinib 2013), anti-PD1 antibodies (nivolumab 2014, pembrolizumab 2014), anti-CTLA-4 antibody (ipilimumab 2011), or peginterferon-alfa-2b (2011) intended to be used in most advanced cases of melanoma.
[Modern methods of molecular targeted therapy for disseminated melanoma].
Review
New
Akhaeva et al., In Vopr Onkol, Dec 2014
New classes of pharmaceuticals appeared in daily clinical practice: inhibitors of MAPK pathway components (BRAF inhibitors vemurafenib and dabrafenib, MEK--inhibitors trametinib and cobimetinib) and immune checkpoint inhibitors that modulate immunologic synapse activity.
Perspective of Targeting Cancer-Associated Fibroblasts in Melanoma.
Review
New
Zhang et al., Cincinnati, United States. In J Cancer, Dec 2014
Although a great deal of progress has been made in the past decade, including the development of immunotherapy using immune checkpoint inhibitors and targeted therapy using BRAF, MEK or KIT inhibitors, treatment for unresectable stage III, stage IV, and recurrent melanoma is still challenging with limited response rate, severe side effects and poor prognosis, highlighting an urgent need for discovering and designing more effective approaches to conquer melanoma.
Targeted next-generation sequencing reveals high frequency of mutations in epigenetic regulators across treatment-naïve patient melanomas.
New
Lian et al., Boston, United States. In Clin Epigenetics, Dec 2014
The most frequently mutated genes were BRAF, MECOM, NRAS, TP53, MLL2, and CDKN2A.
A Subset of Nuclear Receptors are Uniquely Expressed in Uveal Melanoma Cells.
New
Martinez et al., Dallas, United States. In Front Endocrinol (lausanne), Dec 2014
Previous studies of UM cancers identified key mutations in three genes: GNAQ, GNA11, and BRAF.
Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations.
Dummer et al., Zürich, Switzerland. In Ejc Suppl, 2013
Melanoma today is considered as a spectrum of melanocytic malignancies characterised by clinical and molecular features, including targetable mutations in several kinases such as BRAF or c-KIT.
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.
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