Abstract：
:Approximately 75% of melanomas have known driver oncogenic mutations in BRAF, NRAS, GNA11 or GNAQ, while the mutations providing constitutive oncogenic signaling in the remaining melanomas are not known. We established a melanoma cell line from a tumor with none of the common driver mutations. This cell line demonstrated a signaling profile similar to BRAF-mutants, but lacked sensitivity to the BRAF inhibitor vemurafenib. RNA-seq mutation data implicated CRAF R391W as the alternative driver mutation of this melanoma. CRAF R391W was homozygous and over expressed. These melanoma cells were highly sensitive to CRAF, but not BRAF knockdown. In reconstitution experiments, CRAF R391W, but not CRAF WT, transformed NIH3T3 cells in soft-agar colony formation assays, increased kinase activity in vitro, induced MAP kinase signaling and conferred vemurafenib resistance. MAP kinase inducing activity was dependent on CRAF dimerization. Thus, CRAF is a bona fide alternative oncogene for BRAF/NRAS/GNAQ/GNA11 wild type melanomas.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Atefi M,Titz B,Tsoi J,Avramis E,Le A,Ng C,Lomova A,Lassen A,Friedman M,Chmielowski B,Ribas A,Graeber TGdoi
10.1038/srep27454subject
Has Abstractpub_date
2016-06-08 00:00:00pages
27454issn
2045-2322pii
srep27454journal_volume
6pub_type
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