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Titolo:
INTERFERON-GAMMA-INDUCIBLE-PROTEIN-10 (IP-10) IS AN ANGIOSTATIC FACTOR THAT INHIBITS HUMAN NONSMALL CELL LUNG-CANCER (NSCLC) TUMORIGENESIS AND SPONTANEOUS METASTASES
Autore:
ARENBERG DA; KUNKEL SL; POLVERINI PJ; MORRIS SB; BURDICK MD; GLASS MC; TAUB DT; IANNETTONI MD; WHYTE TI; STRIETER RM;
Indirizzi:
UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,DIV PULM & CRIT CARE,3916 TAUBMAN CTR,BOX 0360 ANN ARBOR MI 48109 UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,DIV PULM & CRIT CARE ANN ARBOR MI 48109 UNIV MICHIGAN,SCH DENT,SECT ORAL PATHOL ANN ARBOR MI 48109 UNIV MICHIGAN,DEPT PATHOL ANN ARBOR MI 48109 NCI,MOL IMMUNOREGULAT LAB FREDERICK MD 21702 UNIV MICHIGAN,DEPT SURG,THORAC SURG SECT ANN ARBOR MI 48109
Titolo Testata:
The Journal of experimental medicine
fascicolo: 3, volume: 184, anno: 1996,
pagine: 981 - 992
SICI:
0022-1007(1996)184:3<981:I(IAAF>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
NORMAL HUMAN KERATINOCYTES; PLATELET FACTOR-IV; X-C CHEMOKINE; TUMOR-GROWTH; IN-VIVO; BRONCHOGENIC-CARCINOMA; INDUCED ANGIOGENESIS; ALPHA-INTERFERON; GENE-EXPRESSION; T-CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
D.A. Arenberg et al., "INTERFERON-GAMMA-INDUCIBLE-PROTEIN-10 (IP-10) IS AN ANGIOSTATIC FACTOR THAT INHIBITS HUMAN NONSMALL CELL LUNG-CANCER (NSCLC) TUMORIGENESIS AND SPONTANEOUS METASTASES", The Journal of experimental medicine, 184(3), 1996, pp. 981-992

Abstract

The success of solid tumor growth and metastasis is dependent upon angiogenesis. Neovascularization within the tumor is regulated, in part,by a dual and opposing system of angiogenic and angiostatic factors. We now report that IP-10, a recently described angiostatic factor, is a potent angiostatic factor that regulates non-small cell lung cancer (NSCLC)-derived angiogenesis, tumor growth, and spontaneous metastasis. We initially found significantly elevated levels of IP-10 in freshlyisolated human NSCLC samples of squamous cell carcinoma (SCCA). In contrast, levels of IP-10 were equivalent in either normal lung tissue or adenocarcinoma specimens. The neoplastic cells in specimens of SCCA were the predominant cells that appeared to express IP-10 by immunolocalization. Neutralization of IP-10 in SCCA tumor specimens resulted inenhanced tumor-derived angiogenic activity. Using a model of human NSCLC tumorigenesis in SCID mice, we found that NSCLC tumor growth was inversely correlated with levels of plasma or tumor-associated IP-10. IP-10 in vitro functioned as neither an autocrine growth factor nor as an inhibitor of proliferation of the NSCLC cell lines. Reconstitution of intratumor IP-10 for a period of 8 wk resulted in a significant inhibition of tumor growth, tumor-associated angiogenic activity and neovascularization, and spontaneous lung metastases; whereas, neutralization of IP-10 for 10 wk augmented tumor growth. These findings support the notion that tumor-derived IP-10 is an important endogenous angiostatic factor in NSCLC.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 08:18:48