HER2 overexpression increases sensitivity to gefitinib, an epidermal growth factor receptor tyrosine kinase inhibitor, through inhibition of HER2/HER3 heterodimer formation in lung cancer cells

Cancer Research

Volumn 65, Issue 10, 2005, Pages 4253-4260

  Hirata, Akira ^a   Hosoi, Fumihito ^b   Miyagawa, Miho ^a   Ueda, Shu Ichi ^a   Naito, Seiji ^a   Fujii, Teruhiko ^b   Kuwano, Michihiko ^b   Ono, Mayumi ^a  

^a KYUSHU UNIVERSITY   (Japan)

^b KURUME UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

COMPLEMENTARY DNA; CYCLIN DEPENDENT KINASE INHIBITOR 1B; DIMER; EPIDERMAL GROWTH FACTOR RECEPTOR; EPIDERMAL GROWTH FACTOR RECEPTOR 2; EPIDERMAL GROWTH FACTOR RECEPTOR KINASE INHIBITOR; GEFITINIB; HER3 PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; ONCOPROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; PROTEIN P85ALPHA; UNCLASSIFIED DRUG;

ARTICLE; CANCER CELL CULTURE; CANCER COMBINATION CHEMOTHERAPY; CANCER INHIBITION; CELL CLONE; CELL CYCLE; CELL CYCLE G1 PHASE; CELL CYCLE S PHASE; CELL STRAIN LK2; CELL STRAIN PC9; CONTROLLED STUDY; DIMERIZATION; DRUG CYTOTOXICITY; DRUG EFFICACY; DRUG SENSITIVITY; DRUG TARGETING; ENZYME ACTIVATION; EXON; GENE DELETION; GENE OVEREXPRESSION; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; LUNG CANCER; LUNG NON SMALL CELL CANCER; MONOTHERAPY; ONCOGENE NEU; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; PROTEIN PROTEIN INTERACTION; SIGNAL TRANSDUCTION;

ANTINEOPLASTIC AGENTS; CELL CYCLE PROTEINS; CELL LINE, TUMOR; CYCLIN-DEPENDENT KINASE INHIBITOR P27; DOSE-RESPONSE RELATIONSHIP, DRUG; G1 PHASE; HUMANS; LUNG NEOPLASMS; PHOSPHORYLATION; PROTEIN KINASE INHIBITORS; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; QUINAZOLINES; RECEPTOR, EPIDERMAL GROWTH FACTOR; RECEPTOR, ERBB-2; RECEPTOR, ERBB-3; TRANSFECTION; TUMOR SUPPRESSOR PROTEINS;

EID: 20144377465     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-04-2748     Document Type: Article

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