Significant augmentation of pro-apoptotic gene therapy by pharmacologic bcl-xl down-regulation in mesothelioma

Cancer Gene Therapy

Volumn 8, Issue 8, 2001, Pages 547-554

  Mohiuddin, I ^a   Cao, X ^a   Fang, B ^a   Nishizaki, M ^a   Smythe, W R ^a  

^a UNIVERSITY OF TEXAS MD ANDERSON CANCER CENTER   (United States)

Author keywords

Bak; Bax; bcl 2; bcl xl; Gene therapy; Mesothelioma; p53; Sodium butyrate

Indexed keywords

ACTIN; BUTYRIC ACID; PROTEIN BAK; PROTEIN BCL 2; PROTEIN BCL X; PROTEIN P53; RECOMBINANT PROTEIN; VIRUS VECTOR;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; CANCER INHIBITION; CELL DEATH; CONTROLLED STUDY; GENE INDUCTION; GENE THERAPY; HUMAN; HUMAN CELL; MALIGNANT MESOTHELIOMA; PRIORITY JOURNAL; PROTEIN SYNTHESIS INHIBITION; VIRUS RECOMBINANT;

ADENOVIRIDAE; APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; BCL-X PROTEIN; BISBENZIMIDE; BLOTTING, WESTERN; BUTYRATES; CELL SURVIVAL; COMBINED MODALITY THERAPY; DOWN-REGULATION; FLOW CYTOMETRY; FORMAZANS; GENE THERAPY; HUMANS; IN SITU NICK-END LABELING; MEMBRANE PROTEINS; MESOTHELIOMA; MUTATION; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; TUMOR CELLS, CULTURED; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0034874520     PISSN: 09291903     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.cgt.7700332     Document Type: Article

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