Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
B7.1 expression eliminates tumor resistance to IL-12 gene therapy
Autore:
Heise, CP; Shi, FS; Albertini, MR; Mahvi, DM;
Indirizzi:
Univ Wisconsin Hosp & Clin, Dept Surg, Madison, WI 53792 USA Univ Wisconsin Hosp & Clin Madison WI USA 53792 rg, Madison, WI 53792 USA Univ Wisconsin Hosp & Clin, Dept Med, Madison, WI 53792 USA Univ WisconsinHosp & Clin Madison WI USA 53792 ed, Madison, WI 53792 USA
Titolo Testata:
CANCER GENE THERAPY
fascicolo: 2, volume: 8, anno: 2001,
pagine: 118 - 127
SICI:
0929-1903(200102)8:2<118:BEETRT>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOGENESIS IN-VIVO; T-CELLS; COSTIMULATORY MOLECULES; ANTITUMOR IMMUNITY; B7-1 EXPRESSION; MURINE TUMORS; INTERLEUKIN-12; CTLA-4; CD28; REGRESSION;
Keywords:
gene therapy; interleukin-12; B7.1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Mahvi, DM Univ Wisconsin, Dept Surg, 600 Highland Ave, Madison, WI 53792 USA Univ Wisconsin 600 Highland Ave Madison WI USA 53792 I 53792 USA
Citazione:
C.P. Heise et al., "B7.1 expression eliminates tumor resistance to IL-12 gene therapy", CANC GENE T, 8(2), 2001, pp. 118-127

Abstract

IL-12 gene therapy results in tumor regression in some, but not all, murine models. We hypothesized chat expression of B7.1 on the tumor cell surfacewas necessary for IL-12-mediated tumor regression. In addition, we hypothesized that all cells must express B7.1 for this to be effective. To evaluate this hypothesis, tumor nodules were established in mice with either wild-type B16 melanoma or with B16 melanoma modified to express B7.1. IL-12 cDNAwas transferred to the tumor by particle-mediated gene transfer. All tumors modified to express B7.1 regressed completely after IL-12 cDNA treatment. When the percent of B7.1-transfected B16 cells was decreased to 50%, no animals survived after treatment. Animals rendered tumor-free were then challenged with wild-type B16. Fifty percent of mice was protected from this tumor challenge. Expression of CD28 (the stimulatory B7.1 ligand) was significantly increased in both CD8(+) T cells and natural killer cell populations of mice rejecting tumor challenge compared to mice with tumor growth. Theseresults suggest that the costimulatory molecule B7.1 is required for initial tumor sensitivity to IL-12 gene therapy and that protection from subsequent challenge with B7.1(-) tumor is mediated by CD28(+) immune effector cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 09:20:45