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. 2020 Oct 12;12(10):2935. doi: 10.3390/cancers12102935

Figure 6.

Figure 6

Potential druggability of genetic events represented by 5 mouse models vs. HNC patient tumors (N = 510). (A) Pie chart showing 55% (53/96 genes) of druggable candidates are mutated or copy number altered in 5 mouse models. (B) Pie chart showing 13% of druggable events harbored by 5 metastatic mouse models are genes in the RTK signaling, followed by DNA repair pathway, other unclassified mutations, MAPK pathway, FA pathway, PI3K pathway, immune evasion machinery, JAK/STAT pathway, epigenetic regulatory machinery, and Notch pathway. (C) Mapping of mutation sites of ERBB4 represented by HNC patient tumors (upper) and the 5 mouse models in the tyrosine kinase domain (lower). (D) Summary mapping of aberrations of druggable candidates in 5 mouse models based on the RTK, MAPK, PI3K, NOTCH, JAK/STAT, and DNA damage/cell cycle-related pathways.