MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study.

By P. Ascierto, D. Schadendorf, C. Berking, S. Agarwala, C. V. van Herpen, P. Queirolo, C. Blank, A. Hauschild, J. Beck, A. St-Pierre and 5 more. The Lancet Oncology, 2013

625 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c99a3c3000429554721a3d5d3e41fdc387e98908

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Citations in the corpus

Integrated Proteogenomic Characterization of Clear Cell Renal Cell Carcinoma (2019, background): “Independent of current first-line regimens and immune checkpoint inhibition, the ubiquitous activation of EGFR and downstream signaling cascades (MAPK1), as well as cell-cycle checkpoint regulation (WEE1-CDK1) revealed by our phosphoproteomic analysis, provide additional therapeutic targets that hav”
Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “331,337,521 However, the rapid development of drug resistance has limited the use of these drugs in cancer therapy, resulting in temporary bene ﬁ ts lasting from several months to less than 2 years.”
Comprehensive Characterization of Cancer Driver Genes and Mutations (2018, background): “…are present in 8%of samples and could be sensitive to MEK inhibitors via repurposing; some NRAS mutations are sensitive in SKCM to MEK inhibition in clinical trials, particularly when combined with CDK4 inhibition (Adjei et al., 2008; Ascierto et al., 2013; Dummer et al., 2017; Iams et al., 2017).”
Cutaneous melanoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up†. (2019, background): “There are early signals from a phase II clinical trial that patients with metastatic melanomas, carrying NRAS mutation, may benefit from MEK kinase-inhibitor therapy [40].”
Nivolumab and Ipilimumab versus Ipilimumab in Untreated Melanoma (2015, unknown): “Stable disease 9 (12) 13 (35) 3 (13) 1 (10)”