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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Cancer Discov. 2013 Nov 21;4(1):80–93. doi: 10.1158/2159-8290.CD-13-0642

Figure 1.

Figure 1

Core melanoma escape pathways during disease progression on BRAF Inhibitor therapy. A, Representative photographs (patient #25) of initial vemurafenib response, incomplete response or residual and later acquired BRAFi resistance, which occurred at a site of incompletely shrunken tumor. B, The relative distribution of MAPK-reactivating mechanisms among disease progressive melanomas where such mechanisms were detected. C, The relative distribution of core pathways (MAPK vs. PI3K-PTEN-AKT) and hitherto unknown mechanisms among all melanomas featuring disease progression. D, Non-synonymous mutations in the PI3K-PTEN-AKT core drug escape pathway detected only in disease progression (DP) tumors. The schematics show the locations of mutations in the protein domain structures and their corresponding source patients and tissues. E, Signaling schematics of PI3K-PTEN-AKT pathway components mutated in biopsies of growing melanomas with acquired BRAF inhibitor resistance (PIK3CA, p110; PIK3R2, p85). F, Focal copy number loss of PTEN in DP melanoma of patient #11.