We surveyed data obtained from 408 MIBC tumor samples previously classified into broad molecular phenotypes with distinct median overall survival periods (N, BS, L, LI and LP; [22]) for potentially oncogenic TK alterations, such as amplification and overexpression that might underlie catalytic overactivity, and for coincident overexpression of receptor TKs and their cognate ligands. Here, TKT is linked to neoplasm.