ARTICLE;
CANCER INHIBITION;
CELL VIABILITY;
DRUG EFFICACY;
DRUG SELECTIVITY;
GASTROINTESTINAL STROMAL TUMOR;
HIGH THROUGHPUT SCREENING;
HUMAN;
LUNG CANCER;
NONHUMAN;
PROTEIN PHOSPHORYLATION;
XENOGRAFT;
ANIMAL;
DRUG ANTAGONISM;
GENETICS;
MUTATION;
NOTE;
ANIMALS;
HUMANS;
MUTATION;
PROTEIN KINASE INHIBITORS;
RECEPTOR, EPIDERMAL GROWTH FACTOR;
A specifi c inhibitor of the epidermal growth factor receptor tyrosine kinase
Fry DW, Kraker AJ, McMichael A, Ambroso LA, Nelson JM, Leopold WR, et al. A specifi c inhibitor of the epidermal growth factor receptor tyrosine kinase. Science 1994; 265: 1093-5.
Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefi tinib
Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefi tinib. N Engl J Med 2004; 350: 2129-39.
EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefi tinib and erlotinib
Pao W, Miller V, Zakowski M, Doherty J, Politi K, Sarkaria I, et al. EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefi tinib and erlotinib. Proc Natl Acad Sci U S A 2004; 101: 13306-11.
The EGFR T790M mutation in acquired resistance to an irreversible second-generation EGFR inhibitor
Kim Y, Ko J, Cui Z, Abolhoda A, Ahn JS, Ou SH, et al. The EGFR T790M mutation in acquired resistance to an irreversible second-generation EGFR inhibitor. Mol Cancer Ther 2012; 11: 784-91.
