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. Author manuscript; available in PMC: 2014 Aug 29.
Published in final edited form as: Cell. 2013 Aug 29;154(5):1151–1161. doi: 10.1016/j.cell.2013.08.003

Figure 2. Genetic dependencies targeted by small molecules.

Figure 2

The distribution of CCL response (AUC values) to compound treatment is represented as a heatmap denoting sensitivity (red) or unresponsiveness (blue) aligned with genomic alterations for corresponding CCLs (gray bars). The resource identified known clinically drug-targeted genetic dependencies (A) and known drug-resistance mechanisms (BRAF V600E outlier cell lines: *RKO; #SKMEL28). The resource also suggests dependencies with both mutation and copy number variation in MYC (B). Global analysis of the resource showed EGFR-mutated CCLs are unresponsive to NAMPT inhibitors (C). CNV-H: high-copy number (≥8 copies), TES: all targeted-exome sequencing mutant calls, TES-A: targeted-exome sequencing, non-neutral missense mutations; Onco: Oncomap mutant calls, MUT: any mutation call. See also Figure S2, Table S2, User Guide S1, and Table S3.