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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Clin Cancer Res. 2012 Jan 10;18(5):1472–1482. doi: 10.1158/1078-0432.CCR-11-2906

Figure 4. Relative frequencies of crizotinib resistance mechanisms in ALK+ NSCLC patients and models for potential mechanisms of alternate oncogene acquisition.

Figure 4

(A) The wedges represent different molecular mechanisms of resistance identified in ALK+ NSCLC patients in this study. The blue arc represents presumed or confirmed presence of an alternate oncogene. The yellow arc represents copy number gain (CNG). The red arc represents the presence of an ALK kinase domain mutation. The grey wedge represents those patients where an ALK gene rearrangement was observed, but no mechanism of resistance was identified. *Denotes inclusion of one patient with intrinsic resistance within this category. (B) Model #1 depicts the low level presence of a second oncogenic driver in the same cell as an ALK gene rearrangement, which following treatment with crizotinib becomes the dominant clone. Model #2 depicts the presence of separate clonal populations, some with an ALK gene rearrangement as the driver and others with an alternate oncogene driver (e.g., KRAS or EGFR). Following treatment with crizotinib, the non-ALK clones become the dominant clone.