Guilty as charged: B-RAF is a human oncogene.

By Mathew Garnett, R. Marais. Cancer Cell, 2004

864 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6499f9c5a267291930ee64e2c48dcb11f768ceef

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In Molecular Biology

1. R. Shaw
2. Alec C. Kimmelman
3. Ping Wee
4. Zhixiang Wang
5. R. Roskoski
6. R. DePinho
7. N. Bardeesy
8. Walter Kolch

Citations in the corpus

• Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “B-Raf kinases, key kinases intimately involved in cancer cell proliferation [252], are also inhibited by natural plant compounds such as curcumin, luteolin, quercetin and ursolic acid [253, 254].”
• MAP kinase signalling pathways in cancer (2007, background): “The V600E mutation drastically elevates B-Raf kinase activity and its ability to activate the ERK pathway, as do most other of the cancer-associated mutations (Garnett and Marais, 2004).”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “Interestingly, B-RAF and RAS mutations appear to be mutually exclusive in these cancers (Davies et al. 2002; Garnett and Marais 2004).”
• Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers (2006, background): “The V600 mutation in A-loop is the most frequent type of BRAF mutation in human cancers.(35) Interestingly, this mutation occurs in a similar position to the L861Q mutation in EGFR, and this mutation is present in the viable germline dark skin 5 mutation in the mouse.”
• Is It Reliable to Take the Molecular Docking Top Scoring Position as the Best Solution without Considering Available Structural Data? (2018, background): “It is one of the most frequently mutated genes in human cancers [59]; therefore, therapeutic inhibition of oncogenic B-Raf kinase activity is considered a promising strategy to treat cancer [60].”
• Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “So, the PI(3)K heterodimer is recruited to the membrane to generate local pools of PtdIns(3,4,5)P3.”
• ERK1/2 MAP kinases: structure, function, and regulation. (2012, background): “AF occur in perhaps 7% of all human cancers [26,27].”
• Roles of the RAF/MEK/ERK and PI3K/PTEN/AKT pathways in malignant transformation and drug resistance. (2006, background): “In some models, wild-type (WT) and mutant B-Raf activates Raf-1, which in turn activates MEK and ERK (Garnett and Marais, 2004).”
• Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “It has been estimated that activating mutations of RAF occur in ~7% of all human cancers, with gain-of-function B-RAF mutations being largely associated with melanomas [176,177].”
• Sorafenib in advanced melanoma: a Phase II randomised discontinuation trial analysis (2006, background): “This increased ERK activity may be the consequence of activating BRAF mutations, which are present in up to 80% of human melanomas (Davies et al, 2002; Chang et al, 2004; Garnett and Marais, 2004).”
• Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “This common cancer-derived mutant protein kinase can contribute to oncogenic transformation if placed in the context of additional genetic lesions (Davies et al., 2002; Gar- nett and Marais, 2004).”