| Data show that depletion of SRY (sex determining region Y)-box 10 protein (SOX10) sensitizes mutant proto-oncogene proteins B-raf (BRAF) melanoma cells to RAF inhibitors in vitro and in vivo. | skin, |
| KRAS wild-type metastatic colorectal cancer patients with mutant type proto-oncogene proteins B-raf receiving an epidermal growth factor receptor monoclonal antibody (anti-EGFR) inhibitor as first-line therapy have significantly lower overall response rate, shorter progression-free survival and overall survival. | colorectal, |
| the LMO7-BRAF fusion behaves as an oncogenic alteration in papillary thyroid carcinoma | thyroid, |
| This multicenter retrospective study investigated the effectiveness of BRAF inhibitors (BRAFi) and stereotactic radiosurgery in the combined treatment regimen of intracranial melanoma metastases patients with know B-Raf proto-oncogene serine/threonine kinase 94 kDa (BRAF) mutant status. | skin, |
| these data demonstrate that an oncogene-specific decoupling of mTOR from AMPK or AKT signaling accounts for alterations of resistance mechanisms and metabolic phenotypes. Indeed the inhibition of mTOR in BRAF(V600E) cells counteracts the metabolic predisposition and demonstrates mTOR as a potential target in BRAF(V600E)-driven colorectal carcinomas. | colorectal, |
| Bap1 deletion in melanocytes cooperates with the constitutively active, oncogenic form of BRAF (BRAF(V600E) ) and Ultraviolet rays to cause melanoma in mice. | skin, |
| Studied NRAS and B-Raf proto-oncogene serine/threonine kinase (BRAF) mutations in Turkish cutaneous melanoma patients and their association with clinical stage of the melanomas. | skin, |
| introducing a rapid and sensitive microarray-based assay for the multiplex detection of minority mutations of oncogenes (KRAS, NRAS and BRAF) with relevant diagnostics implications in tissue biopsies and plasma samples in metastatic colorectal cancer patients | colorectal, |
| Aging-like acquisition of DNA methylation favors survival of cells with BrafV600E mutationcby suppressing senescence and activating stem cell pathways and predispositing to oncogene-driven colon tumorigenesis. | colorectal, |
| results suggest that miR-10b is an important mediator of oncogenic B-RafV600E activity in melanoma. | skin, |
| Inhibiting BRAF Oncogene-Mediated Radioresistance Effectively Radiosensitizes BRAF(V600E)-Mutant Thyroid Cancer Cells by Constraining DNA Double-Strand Break Repair. | thyroid, |
| A subset of endosalpingiotic lesions are clonal and harbour the same oncogenic driver mutations in BRAF shared with low-grade ovarianserous tumours. | ovarian, |
| Genetic deregulation of TET DNA demethylases by oncogenic BRAFV600E was responsible for CpG-island methylator phenotype (CIMP) cancer initiation in the colon. | colorectal, |
| Oncogenic BRAF, endoplasmic reticulum stress, and autophagy: Crosstalk and therapeutic targets in cutaneous melanoma. | skin, |
| Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf. | None |
| Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. | None |
| Switching on kinases: oncogenic activation of BRAF and the PDGFR family. | None |
| Guilty as charged: B-RAF is a human oncogene. | None |
| REVIEW: our understanding of B-RAF as an oncogene and of its role in cancer | None |
| B-raf mutations surrounding Thr439 found in human cancers are unlikely to contribute to increased oncogenic properties of B-raf | None |