KRAS-mutated non-small cell lung cancer cells are responsive to either co-treatment with erlotinib or gefitinib and histone deacetylase inhibitors or single treatment with lapatinib

Oncology Reports

Volumn 25, Issue 4, 2011, Pages 1021-1029

  Kurtze, Ina ^a   Sonnemann, Jürgen ^a   Beck, James F ^a  

^a JENA UNIVERSITY HOSPITAL   (Germany)

Author keywords

Apoptosis; Erlotinib; Gefitinib; Histone deacetylase inhibitors; Lapatinib; Non apoptotic cell death; Non small cell lung cancer

Indexed keywords

BUTYRIC ACID; ERLOTINIB; GEFITINIB; K RAS PROTEIN; LAPATINIB; VORINOSTAT;

APOPTOSIS; ARTICLE; CANCER CELL; CELL DEATH; CONCENTRATION RESPONSE; DEPOLARIZATION; DRUG POTENTIATION; FLUORESCENCE MICROSCOPY; GENE MUTATION; LUNG NON SMALL CELL CANCER; MITOCHONDRIAL MEMBRANE POTENTIAL; PRIORITY JOURNAL; TREATMENT RESPONSE;

ADENOCARCINOMA; ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CELL PROLIFERATION; FLOW CYTOMETRY; HISTONE DEACETYLASE INHIBITORS; HUMANS; HYDROXAMIC ACIDS; LUNG NEOPLASMS; MEMBRANE POTENTIAL, MITOCHONDRIAL; MUTATION; PROTO-ONCOGENE PROTEINS; QUINAZOLINES; RAS PROTEINS; TUMOR CELLS, CULTURED;

EID: 79952207890     PISSN: 1021335X     EISSN: 17912431     Source Type: Journal    
DOI: 10.3892/or.2011.1160     Document Type: Article

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