ArticleMolecular cancer research : MCR2014
Beneficial effects of RAF inhibitor in mutant BRAF splice variant-expressing melanoma.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Conquering oncogenic KRAS and its bypass mechanisms.Theranostics · 2022Review
- BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association.Cell reports · 2018Article
- A novel RFLP-ARMS TaqMan PCR-based method for detecting the BRAF V600E mutation in melanoma.Oncology letters · 2018Article
- Response and Resistance to Paradox-Breaking BRAF Inhibitor in MelanomasMolecular cancer therapeutics · 2018Article
- Bioinformatics analysis of gene expression alterations conferring drug resistance in tumor samples from melanoma patients with EGFR-activatingOncology letters · 2018Article
- Visualization of RAS/MAPK Signaling In Situ by the Proximity Ligation Assay (PLA).Methods in molecular biology (Clifton, N.J.) · 2017Article
- Structural characterization of NRAS isoform 5.Protein science : a publication of the Protein Society · 2016Article
- Of Mice and Melanoma: PDX System for Modeling Personalized Medicine.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Fibroblast-derived neuregulin 1 promotes compensatory ErbB3 receptor signaling in mutant BRAF melanoma.The Journal of biological chemistry · 2015Article
- Tumor heterogeneity and plasticity as elusive drivers for resistance to MAPK pathway inhibition in melanoma.Oncogene · 2015Review
- Article
- Beyond BRAF: where next for melanoma therapy?British journal of cancer · 2015Review
- Perspective of Targeting Cancer-Associated Fibroblasts in Melanoma.Journal of Cancer · 2015Review
- Review
- Adaptive resistance to RAF inhibitors in melanoma.Pigment cell & melanoma research · 2014Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
unlabelledResistance to RAF inhibitors such as vemurafenib and dabrafenib is a major clinical problem in the treatment of melanoma. Patients with mutant BRAF melanoma that progress on RAF inhibitors have limited treatment options, and drug removal from resistant tumors may elicit multiple effects. A frequent mechanism of resistance to RAF inhibitors is caused by expression of mutant BRAF splice variants. RAF inhibitor-resistant cell lines, generated in vivo, were tested as to whether or not mutant BRAF splice variants confer a fitness advantage in the presence of RAF inhibitor. Critically, cells expressing distinct mutant BRAF splice variants grow more efficiently in vitro and in vivo in the presence of the vemurafenib analog, PLX4720, compared with in the absence of inhibitor. PLX4720-treated BRAF splice variant-expressing cells exhibited levels of phospho-extracellular signal-regulated kinase (ERK)1/2 comparable to untreated parental cells. In addition, a reduction in phospho-ERK1/2 levels following treatment with the MEK inhibitor, trametinib (GSK1120212) phenocopied the fitness benefit provided by PLX4720. These data indicate that mutant BRAF splice variant-expressing melanoma cells are benefited by defined concentrations of RAF inhibitors. IMPLICATIONS: This study provides evidence that RAF inhibitor-resistant melanoma cells benefit from continued therapy.
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