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Titolo:
Development of a syngenic murine B16 cell line-derived melanoma susceptible to destruction by neuroattenuated HSV-1
Autore:
Miller, CG; Krummenacher, C; Eisenberg, RJ; Cohen, GH; Fraser, NW;
Indirizzi:
Univ Penn, Sch Med, Dept Microbiol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Microbiol, Philadelphia, PA 19104 USA Univ Penn, Sch Dent Med, Ctr Oral Hlth Res, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Hlth Res, Philadelphia, PA 19104 USA Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Pathobiol, Philadelphia, PA 19104 USA
Titolo Testata:
MOLECULAR THERAPY
fascicolo: 2, volume: 3, anno: 2001,
pagine: 160 - 168
SICI:
1525-0016(200102)3:2<160:DOASMB>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
HERPES-SIMPLEX VIRUS; SUICIDE GENE-THERAPY; FACTOR RECEPTOR SUPERFAMILY; EXPERIMENTAL BRAIN-TUMORS; LONG-TERM SURVIVAL; POLIOVIRUS RECEPTOR; ENTRY MEDIATOR; GLYCOPROTEIN-D; MALIGNANT-MELANOMA; PSEUDORABIES VIRUS;
Keywords:
HSV-1; tumor model; melanoma; gene therapy; Hve receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Fraser, NW 3610 Hamilton Walk,319 Johnson Pavil, Philadelphia, PA 19104 USA 3610 Hamilton Walk,319 Johnson Pavil Philadelphia PA USA 19104
Citazione:
C.G. Miller et al., "Development of a syngenic murine B16 cell line-derived melanoma susceptible to destruction by neuroattenuated HSV-1", MOL THER, 3(2), 2001, pp. 160-168

Abstract

HSV-1 ICP34.5 mutants can slow progression of preformed tumors in rodent models. However, the current models available for study are limited due to the lack of a syngenic, low-immunogenic tumor model susceptible to HSV-1. Thus we have developed a new model to determine the role of the immune response in viral-mediated tumor destruction. The human herpesvirus entry (Hve) receptors (HveA, HveB, and HveC) and a control plasmid were transfected intoB78H1 murine melanoma cells. Transfection of HveA and HveC conferred sensitivity to HSV-1 to these cells. A10 (HveA), C10 (HveC), and control cells were able to form tumors reproducibly in vivo. The transfection of the receptors into B78H1 cells did not induce a detectable in vivo immunogenicity tothe tumors. Finally, A10 and C10 tumor-bearing mice treated with HSV-1 1716 had significant prolongation of survival compared to mock-treated mice. These data suggest that A10 and C10 will be useful as in vivo models for studying the role of the immune response in viral-mediated tumor destruction.

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Documento generato il 26/02/20 alle ore 04:50:20