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. 2016 Sep 29;7:312. doi: 10.3389/fphar.2016.00312

FIGURE 1.

FIGURE 1

cBioPortal data visualization and analysis. (A) Genomic alteration frequency in the BRAF gene in 123 cancer patient studies, NCI-60 and CCLE-883 cancer cell lines. (B) Oncoprint showing frequencies of genomic alterations observed in BRAF, N-RAS, and c-KIT gene in 278 tumor samples in the TCGA skin cutaneous melanoma. (B) The panel shows that 143 (51%) of patients of the skin cutaneous melanoma TCGA study had one or more BRAF alterations. (C) The panel shows a genomic overview of one patient identified by the number TCGA-ER-A3PL-06. The upper view panel shows copy number variation and the frequency of mutations observed in each chromosome of the patient. The lower view panel shows details of the four top genes from 283 genes in which at least one alteration was identified. (D) The plot shows the correlation between BRAF mRNA expression and the putative copy-number alterations (gain or amplification). In this plot is include the deep or shallow deletion (not mutated, missense and in frame mutation) BRAF mutation. (E) The Kaplan–Meier overall survival curve indicates that the cases with BRAF mutation had higher overall survival than the cases without BRAF alterations. (F) This schematic representation shows the position and hot spot mutations across BRAF protein domains. The missense mutations most frequently observed are V600E, D, K, and R. Inside (G) shows a stick model representation for BRAF kinase domain and molecular inhibitory mechanism proposed to vemurafenib (Zelboraf; Plexxikon/Roche), a small molecule drug approved to treat melanoma patients.