EGFR and neoplasm: These contained a variety of genetic aberrations including: EGFR and KRAS gene mutations and genetic amplification of cMET and FGFR1. Within these models, gefitinib antitumor activity was generally poor, and tumor regression was only observed in a model containing an EGFR exon 19 deletion - consistent with previous preclinical studies and supportive of the current patient selection criteria for EGFR-targeted therapies, such as gefitinib and erlotinib.