Supplementary Figures 1 - 10 from Cetuximab Response of Lung Cancer–Derived EGF Receptor Mutants Is Associated with Asymmetric Dimerization

PDF file - 303K, L704N or I941R cis mutation disrupts constitutive dimerization of mutant EGFR (S1); Tyrosine-phosphorylation is abrogated on L704N or I941R compound mutants of dimerization-dependent mutants (S2); Wild-type EGFR, but not Ex20Ins mutant are dependent on asymmetric dimerization for oncogenic transformation (S3); Tyrosine-phosphorylation on dimerization-independent mutants is significantly impaired by introduction of receiver-impairing or activator-impairing mutation (S4); Cell surface expression levels of various EGFR mutants in NIH-3T3 cells (S5); Activities of receiver monomers and activator monomers of wild-type EGFR (S6); Cell surface expression of mutant EGFR in stable cell lines (S7); Differential pharmacological effects of gefitinib and cetuximab against distinct mutant EGFR (S8); Generation and characterization of bitransgenic mice with inducible expression of EGFR Ex20Ins in lung compartments (S9); Cetuximab downregulates tyrosine phosphorylation on mutant EGFR in mouse tumors (S10).