BRAF and RAS mutations in human lung cancer and melanoma.

By M. Brose, Patricia Volpe, Michael D. Feldman, Madhu S. Kumar, I. Rishi, Renee M Gerrero, E. Einhorn, Meenhard Herlyn, J. Minna, A. Nicholson and 10 more. Cancer Research, 2002

1,126 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b365158b7f4298f8d7f0b559b3d301cee61ac2d5

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Citations in the corpus

• Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer (2010, background): “Approximately 2–3% of NSCLCs harbour mutations in BRAF , which encodes a signalling molecule downstream of EGF”
• Clinical characteristics of patients with lung adenocarcinomas harboring BRAF mutations. (2011, result): “The incidence of BRAF mutations in our series was 3% (95% CI, 2% to 4%), which is similar to other data.(25) Remarkably, all patients with a BRAF mutation were current or former smokers.”
• Discovery and development of sorafenib: a multikinase inhibitor for treating cancer (2006, background): “Constitutive B-Raf activity can be caused by activating oncogenic mutations, such as the b-raf V600E mutation, which is prevalent in melanomas (63%”
• The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, unknown): “This drug also targets against PI3K in solid tumors (124,125), serine/threonine kinase BRAF to treat melanoma (126-128), the receptor tyrosine kinase EGFR for lung cancer (129,130), and serine/threonine kinase mTOR for the treatment of renal tumors (131).”
• American Society of Clinical Oncology Clinical Practice Guideline update on chemotherapy for stage IV non-small-cell lung cancer. (2009, background): “KRAS mutations are uncommon in squamous cell carcinomas.(160,161) Multiple studies have ASCO Stage IV Non–Small-Cell Lung Cancer Guideline Update”
• Non-small cell lung cancer: current treatment and future advances. (2016, background): “Approximately 10–25% of patients with adenocarcinoma have KRAS mutation-associated tumors (54).”
• Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. (2004, background): “Surovarian (Singer et al., 2003), and papillary thyroid carci-prisingly, three mutants have reduced kinase activity nomas (Brose et al., 2002; Cohen et al., 2003), implicat-towards MEK in vitro but, by activating C-RAF in vivo, ing activating oncogenic mutations of B-RAF as critical signal to ERK…”