Primary resistance to cetuximab in a panel of patient-derived tumour xenograft models: Activation of MET as one mechanism for drug resistance

EGFR mutations. The table shows tumour type and optimal T/C values of the tumours and the EGFR mutations found by MassARRAY analysis of the following EGFR mutations: R108K, T263P, A289V, G598V, E709K/H, E709A/G/V, G719S/C, G719A, M766_A767insAI, S768I, V768_D770insASV, V769_D770insCV, D770_N771>AGG/V769_D770insASV/V769_D770insASV, D770N771insG, N771P772>SVDNR, P772_H773insV, H773>NPY, H773_V774insNPH/PH/H, V774_C775insHV, T790M, L858R, L861Q, E746_T751del, E746_A750del, E756_T751del, S752D, L747_E749del, L747_T750del, L747_S752del, L747_T751del, L747_S752del, P753S, A750P, T751A, T751P, T751I, S752I/F, S752_I759del, L747_Q ins, E746_T751del, I ins (combined), E746_A750del, T751A(combined), L747_E749del, A750P (combined), L747_T750del, P ins (combined), L747_S752del, Q ins(combined).

Details of KRAS Mutations. KRAS mutations are listed with the tumour type and the optimal T/C for in vivo activity of cetuximab of the tumour. The mean optimal T/C value for each KRAS mutation was calculated. Reference: Pearce, M., et al. Mutation profiling in tumour samples using the Sequenom OncoCarta™ Panel. Nature Methods, June 2009, vii.