Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways

Science

Volumn 305, Issue 5687, 2004, Pages 1163-1167

  Sordella, Raffaella ^a   Bell, Daphne W ^a   Haber, Daniel A ^a   Settleman, Jeffrey ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELLS; DRUG PRODUCTS; GROWTH KINETICS; RNA; TUMORS;

APOPTOSIS; LUNG CANCER;

PULMONARY DISEASES;

2 MORPHOLINO 8 PHENYLCHROMONE; APOPTOSIS INHIBITOR; CISPLATIN; DOXORUBICIN; EPIDERMAL GROWTH FACTOR RECEPTOR; FAS LIGAND; GEFITINIB; MITOGEN ACTIVATED PROTEIN KINASE; N BENZYL 2 CYANO 3 (3,4 DIHYDROXYPHENYL)ACRYLAMIDE; PROTEIN KINASE B; PROTEIN TYROSINE KINASE INHIBITOR; SMALL INTERFERING RNA; STAT PROTEIN;

CANCER; MUTATION;

APOPTOSIS; ARTICLE; CELL PROLIFERATION; CELL SURVIVAL; CONTROLLED STUDY; DOSE TIME EFFECT RELATION; DRUG EFFICACY; DRUG MECHANISM; DRUG RECEPTOR BINDING; ENZYME INHIBITION; ENZYME SPECIFICITY; GENE MUTATION; HUMAN; HUMAN CELL; INHIBITION KINETICS; LUNG CANCER; LUNG NON SMALL CELL CANCER; PHARMACOLOGICAL BLOCKING; PRIORITY JOURNAL; PROTEIN DOMAIN; SIGNAL TRANSDUCTION;

ANIMALS; ANTINEOPLASTIC AGENTS; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CATALYTIC DOMAIN; CELL LINE; CELL LINE, TUMOR; CELL SURVIVAL; DNA-BINDING PROTEINS; ENZYME ACTIVATION; HUMANS; LUNG NEOPLASMS; MICE; MILK PROTEINS; MITOGEN-ACTIVATED PROTEIN KINASES; MUTATION; MUTATION, MISSENSE; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; QUINAZOLINES; RECEPTOR, EPIDERMAL GROWTH FACTOR; RNA, SMALL INTERFERING; SEQUENCE DELETION; SIGNAL TRANSDUCTION; STAT5 TRANSCRIPTION FACTOR; TRANS-ACTIVATORS; TRANSFECTION; TYROSINE;

EID: 4143066760     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.1101637     Document Type: Article

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21. We thank P. Harris for technical assistance, T. Lynch and members of the Haber and Settleman laboratories for helpful discussions, and M. Betson for critical comments on the manuscript. This work was supported by grants from the Sandler Family Foundation (to D.A.H. and D.W.B.), NIH (PO1 95281 to D.A.H. and D.W.B.), the Doris Duke Charitable Foundation (to D.A.H.), the Samuel Waxman Cancer Research Foundation (to J.S.), and the Saltonstall Scholarship (to J.S.).