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Titolo:
Interleukin-6 modulated conditionally replicative adenovirus as an antitumor/cytotoxic agent for cancer therapy
Autore:
Rancourt, C; Piche, A; Gomez-Navarro, J; Wang, MH; Alvarez, RD; Siegel, GP; Fuller, GM; Jones, SA; Curiel, DT;
Indirizzi:
Univ Alabama, Gene Therapy Program, Birmingham, AL 35294 USA Univ AlabamaBirmingham AL USA 35294 py Program, Birmingham, AL 35294 USA Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 & Gynecol, Birmingham, AL 35294 USA Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 ept Pathol, Birmingham, AL 35294 USA Univ Alabama, Dept Cell Biol, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 Cell Biol, Birmingham, AL 35294 USA Univ Alabama, Dept Surg, Birmingham, AL 35294 USA Univ Alabama BirminghamAL USA 35294 Dept Surg, Birmingham, AL 35294 USA Univ4,herbrooke, Fac Med, Dept Microbiol & Infectiol, Sherbrooke, PQ J1H 5N Univ Sherbrooke Sherbrooke PQ Canada J1H 5N4 ctiol, Sherbrooke, PQ J1H 5N
Titolo Testata:
CLINICAL CANCER RESEARCH
fascicolo: 1, volume: 5, anno: 1999,
pagine: 43 - 50
SICI:
1078-0432(199901)5:1<43:IMCRAA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN OVARIAN-CARCINOMA; AUTOCRINE GROWTH-FACTOR; RENAL-CELL CARCINOMAS; HUMAN TUMOR-CELLS; SCID MOUSE MODEL; GENE-THERAPY; IN-VITRO; EPITHELIAL CANCER; MALIGNANT GLIOMAS; BREAST-CARCINOMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Curiel, DT Univ35294ama, Gene Therapy Program, 1824 6th Ave S,WTI 620, Birmingham, AL Univ Alabama 1824 6th Ave S,WTI 620 Birmingham AL USA 35294 AL
Citazione:
C. Rancourt et al., "Interleukin-6 modulated conditionally replicative adenovirus as an antitumor/cytotoxic agent for cancer therapy", CLIN CANC R, 5(1), 1999, pp. 43-50

Abstract

In this study, we report that an interleukin-6 (IL-6)-inducible E1A-substituting activity can be exploited for the production of infectious adenoviral particles during infection with the E1A-deleted adenovirus (Ad) Ad5d1312,The basal level of complementation can be increased by 1.5 log by induction of the HepG2 cells with recombinant human IL-6, Additionally, the IL-6-inducible E1A-substituting activity can complement E1A deletion in other cancer cell lines to render them Ad producer cells on induction with recombinant human IL-6, although the efficiency of complementation varies between cell lines. Ad5d1312 can replicate in, produce cytotoxic effect, and kill human tumor cells without addition of exogenous IL-6 in the context of tumor cells possessing an IL-6 autocrine are, such as ovarian tumor cells. In contrast, normal human mesothelial cells isolated from normal human peritoneum lining do not support replication of Ad5d1312, even in the presence of exogenous IL-6, These results suggest that Ad5d1312 could be used as a cytotoxicagent to selectively kill tumor cells responsive to or possessing an IL-6 autocrine arc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 14:22:29