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Titolo:
Impaired tumorigenicity of human pancreatic cancer cells retrovirally transduced with interleukin-12 or interleukin-15 gene
Autore:
Yoshida, Y; Tasaki, K; Miyauchi, M; Narita, M; Takenaga, K; Yamamoto, H; Yamaguchi, T; Saisho, H; Sakiyama, S; Tagawa, M;
Indirizzi:
Chiba Canc Ctr Res Inst, Div Pathol, Chuo Ku, Chiba 2608717, Japan Chiba Canc Ctr Res Inst Chiba Japan 2608717 huo Ku, Chiba 2608717, Japan Chiba Canc Ctr Res Inst, Div Chemotherapy, Chiba 2608717, Japan Chiba CancCtr Res Inst Chiba Japan 2608717 herapy, Chiba 2608717, Japan Chiba Univ, Sch Med, Dept Med 1, Chiba, Japan Chiba Univ Chiba JapanChiba Univ, Sch Med, Dept Med 1, Chiba, Japan Chiba Univ, Sch Med, Dept Surg 2, Chiba, Japan Chiba Univ Chiba JapanChiba Univ, Sch Med, Dept Surg 2, Chiba, Japan Osaka Univ, Fac Pharmaceut Sci, Dept Immunol, Osaka, Japan Osaka Univ Osaka Japan , Fac Pharmaceut Sci, Dept Immunol, Osaka, Japan
Titolo Testata:
CANCER GENE THERAPY
fascicolo: 2, volume: 7, anno: 2000,
pagine: 324 - 331
SICI:
0929-1903(200002)7:2<324:ITOHPC>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
NATURAL-KILLER-CELLS; RECEPTOR-BETA-CHAIN; RECOMBINANT HUMAN INTERLEUKIN-12; IL-2 RECEPTOR; IN-VIVO; ACTIVE IMMUNOTHERAPY; STIMULATORY FACTOR; INTERFERON-GAMMA; T-LYMPHOCYTES; TUMOR-GROWTH;
Keywords:
interleukin-12; interleukin-15; pancreatic cancer; gene therapy; retrovirus vector;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Tagawa, M Chiba Canc Ctr Res Inst, Div Pathol, Chuo Ku, 666-2 Nitona, Chiba 2608717,Japan Chiba Canc Ctr Res Inst 666-2 Nitona Chiba Japan 2608717 ,Japan
Citazione:
Y. Yoshida et al., "Impaired tumorigenicity of human pancreatic cancer cells retrovirally transduced with interleukin-12 or interleukin-15 gene", CANC GENE T, 7(2), 2000, pp. 324-331

Abstract

We examined the antitumor effect of locally secreted interleukin (IL)-12 or IL-15 on human pancreatic cancer cells (AsPC-1). We subcutaneously inoculated AsPC-1 cells retrovirally transduced with IL-12 or IL-15 cDNA into nude mice. Tumors derived from these cells showed retarded growth compared with those from wild-type (wt) cells. Nude mice inoculated intraperitoneally with the cytokine producers survived longer than those injected with wt cells. These cytokine producers were also tested for their tumor growth in severe combined immunodeficient mice. The tumor growth of IL-12 producers was similarly suppressed as found in nude mice, but the average tumor volumes ofIL-15 producers were not statistically different from those of wt tumors. In nude mice that were administered anti-asialo CM, antibody before the inoculation of the tumor cells, growth retardation of tumors of IL-12 producers remained the same as in untreated animals, but that of IL-15 producers was markedly reduced. Immunohistochemical analysis revealed that CD11b(+) cells migrated into the tumors of cytokine producers and that the number of CD31(+) endothelial cells within the tumors was not different between IL-12 producers and wt cells. Taken together with other data, it is possible that granulocytes are candidate cells for the IL-12-mediated antitumor effect, and that natural killer cells and gamma delta T cells are involved in the IL-15-induced antitumor effect. We did not observe synergistic effects of these cytokines to suppress subcutaneous tumors.

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Documento generato il 02/04/20 alle ore 00:13:10