Hypermethylation of the death-associated protein kinase promoter attenuates the sensitivity to TRAIL-induced apoptosis in human non-small cell lung cancer cells. [electronic resource]
Producer: 20050505Description: 685-91 p. digitalISSN:- 1541-7786
- Antimetabolites, Antineoplastic -- pharmacology
- Apoptosis
- Apoptosis Regulatory Proteins
- Azacitidine -- analogs & derivatives
- Calcium-Calmodulin-Dependent Protein Kinases -- biosynthesis
- Carcinoma, Non-Small-Cell Lung -- genetics
- Cell Line, Tumor
- Cloning, Molecular
- Coloring Agents -- pharmacology
- DNA Fragmentation
- DNA Methylation
- DNA, Complementary -- metabolism
- Death-Associated Protein Kinases
- Decitabine
- Dose-Response Relationship, Drug
- Drug Resistance, Neoplasm
- Fas Ligand Protein
- Humans
- Immunohistochemistry
- In Situ Nick-End Labeling
- Lung Neoplasms -- genetics
- Membrane Glycoproteins -- metabolism
- Polymerase Chain Reaction
- Promoter Regions, Genetic
- RNA, Messenger -- metabolism
- Receptors, TNF-Related Apoptosis-Inducing Ligand
- Receptors, Tumor Necrosis Factor -- metabolism
- Reverse Transcriptase Polymerase Chain Reaction
- TNF-Related Apoptosis-Inducing Ligand
- Tetrazolium Salts -- pharmacology
- Thiazoles -- pharmacology
- Time Factors
- Treatment Outcome
- Tumor Necrosis Factor-alpha -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
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