| These findings enhance our understanding of factors cooperating with BRAF inhibition that accelerate keratinocyte oncogenesis as well as broaden the knowledge base of multifactorial mediators of cancer in general. | None |
| oncogenic activation of BRAF allows tumor cells to co-opt an evolutionarily conserved MHC-I trafficking pathway as a strategy to facilitate immune evasion. | None |
| Study reports that mice engineered to overexpress either the full-length murine B-Raf pseudogene Braf-rs1 and its human ortholog, BRAFP1, elicit their oncogenic activity, at least in part, as competitive endogenous RNAs (ceRNAs) that elevate BRAF expression and MAPK activation in vitro and in vivo. | None |
| Studies suggest that the role of tumor biomarker V600E mutation of the BRAF proto-oncogene to detect or exclude cancers in patients with fine-needle aspiration (FNA) reports is marginal and should be reconsidered in guidelines. | None |
| coexpression of BRAF(V600E) and KRAS(G12D) in early tumorigenesis leads to negative selection due to oncogene-induced senescence | None |
| Expression of oncogenic BRAFV600E in melanocytes induces Schwannian differentiation in vivo. | None |
| MIG-6 efficiently reduces cellular transformation driven by oncogenic BRAF by orchestrating a negative feedback circuit directed towards the EGFR. | None |
| Melanocytic nevi excised during B-Raf proto-oncogene (BRAF) inhibitor therapy: A study of 19 lesions from 10 patients. | None |
| Studies indicate that more than half of all Erdheim-Chester disease (ECD) patients carry the proto-oncogene protein B-raf mutation BRAF(V600E) and treated with vemurafenib, a BRAF inhibitor, which has proven highly beneficial. | None |
| Data suggest that core-needle biopsy (CNB) + B-Raf proto-oncogene protein BRAF(V600E) mutation analysis can reduce rates of preventable diagnostic surgery. | None |
| Data indicate that tumors with proto-oncogene proteins BRAF or KRAS mutations were in correlation with elevated serum level of carbohydrate antigen (CA19-9) and carcinoma embryonic antigen (CEA). | None |
| The vast majority of these tumors harbor the oncogenic BRAF V600E mutation. [review] | None |
| This study discovered oncogenic BRAF deletions with a distinct activation mechanism dependent on the BRAF dimer formation in tumor cells. | None |
| Growth arrest is accompanied by MAPK-mediated serine/threonine phosphorylation and suppression of a variety of oncogenic drivers that resist treatment by B-Raf(V600E) kinase inhibitors, including ErbB members, c-Met, IGFR, IRS, STAT3 and Akt. | None |
| these contrasting signatures precisely match those proposed to confer bias toward Hras(CAA61CTA) versus Braf(GTG636GAG) mutations in the original tumor sets. Our findings highlight a novel mechanism whereby exposure history acts through strand-biased mutagenesis to specify activation of preferred oncogenes | None |
| Results show that promoter mutations render telomerase reverse transcriptase (TERT) expression dependent on MAPK signal pathway activation due to oncogenic BRAF or NRAS mutations. | None |
| FZR1 inhibits BRAF oncogenic functions via both APC-dependent proteolysis and APC-independent disruption of BRAF dimers, whereas hyperactivated ERK and CDK4 reciprocally suppress APC(FZR1) E3 ligase activity | None |
| we suggest that screening for somatic BRAF alterations should extend beyond the well-documented hotspot variant BRAF p.V600E, as the pathogenic variant p.T599dup described here mimics the increased oncogenic kinase activity associated with p.V600E | None |
| Oncogenic BRAF positively regulates expression, phosphorylation, and nuclear localization of ERK5. Importantly, ERK5 kinase and transcriptional activities are enhanced by BRAF. | None |
| oncogenic BRAF renders cells refractory to p66ShcS36 phosphorylation, which is essential for p66Shc activation and mitochondrial reactive oxygen species production. | None |