A cell type-specific and gap junction-independent mechanism for the herpes simplex virus-1 thymidine kinase gene/ganciclovir-mediated bystander effect

Clinical Cancer Research

Volumn 5, Issue 11, 1999, Pages 3639-3644

  Princen, Frédéric ^b   Robe, Pierre ^b   Lechanteur, Chantal ^b   Mesnil, Marc ^c   Rigo, Jean Michel ^b   Gielen, Jacques ^b   Merville, Marie Paule ^b   Bours, Vincent ^a,b  

^a UNIVERSITY OF LIÈGE   (Belgium)

^b UNIVERSITY OF LIÈGE   (Belgium)

^c INTERNATIONAL AGENCY FOR RESEARCH ON CANCER   (France)

Author keywords

[No Author keywords available]

Indexed keywords

18ALPHA GLYCYRRHETINIC ACID; GANCICLOVIR; OCTANOL; THYMIDINE KINASE;

ANIMAL CELL; ARTICLE; CANCER CELL CULTURE; CELL COMMUNICATION; CELL SURVIVAL; CONCENTRATION RESPONSE; CULTURE MEDIUM; GAP JUNCTION; GENE TRANSFER; HERPES SIMPLEX VIRUS 1; NONHUMAN; PRIORITY JOURNAL; RAT; SUICIDE GENE;

1-OCTANOL; ADENOCARCINOMA; ANIMALS; ANTIVIRAL AGENTS; CELL COMMUNICATION; CELL SURVIVAL; COLONIC NEOPLASMS; GANCICLOVIR; GAP JUNCTIONS; GENETIC VECTORS; GLYCYRRHETINIC ACID; HERPESVIRUS 1, HUMAN; MOLONEY MURINE LEUKEMIA VIRUS; RATS; THYMIDINE KINASE; TRANSFECTION; TUMOR CELLS, CULTURED;

EID: 0032711633     PISSN: 10780432     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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