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Titolo:
Paradoxical effects of platelet-derived growth factor-A overexpression in malignant mesothelioma - Antiproliferative effects in vitro and tumorigenicstimulation in vivo
Autore:
Metheny-Barlow, LJ; Flynn, B; van Gijssel, HE; Marrogi, A; Gerwin, BI;
Indirizzi:
NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA NCI Bethesda MD USA20892 uman Carcinogenesis Lab, Bethesda, MD 20892 USA NCI, Cellular Carcinogenesis & Tumor Promot Lab, Div Basic Sci, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 omot Lab, Div Basic Sci, Bethesda, MD 20892 USA
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 6, volume: 24, anno: 2001,
pagine: 694 - 702
SICI:
1044-1549(200106)24:6<694:PEOPGF>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR INDUCES APOPTOSIS; PDGF ALPHA-RECEPTORS; SMOOTH-MUSCLE CELLS; PLEURAL MESOTHELIOMA; SIGNAL-TRANSDUCTION; IN-VITRO; EXPRESSION; ASBESTOS; LINES; BETA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Metheny-Barlow, LJ Georgetown Univ, Lombardi canc Ctr, Res Bldg E301,3970 Reservoir Rd NW, Washington, DC 20007 USA Georgetown Univ Res Bldg E301,3970 Reservoir Rd NW Washington DC USA 20007
Citazione:
L.J. Metheny-Barlow et al., "Paradoxical effects of platelet-derived growth factor-A overexpression in malignant mesothelioma - Antiproliferative effects in vitro and tumorigenicstimulation in vivo", AM J RESP C, 24(6), 2001, pp. 694-702

Abstract

Malignant mesothelioma is associated with asbestos exposure and remains resistant to all therapeutic intervention. Previous studies have suggested anenhancing role for platelet-derived growth factor (PDGF) in mesothelial tumorigenicity, although the mechanism by which PDGF facilitates tumorigenicity is unknown. Here, we evaluate the contribution of PDGF-A expression to mesothelial tumorigenicity using ectopic modulation of PDGF-A expression. Wefind, in accordance with other reports, that the receptor for PDGF-A, although expressed at high levels in normal human mesothelial cells, is not easily detectable in mesothelioma. Further, we show that PDGF-A overexpressionis responsible for autocrine downregulation of its receptor. Our data indicate, surprisingly, that for mesothelioma cells in vitro, high-level activation of a PDGF-A-PDGF receptor loop is antiproliferative whereas abrogationof PDGF-A expression stimulates growth. These data suggest that PDGF-A does not contribute to tumorigenicity by autocrine stimulation of proliferation. In contrast, increased PDGF-A expression in vivo increases tumor incidence and growth rate and decreases the latency period to tumor formation whereas abrogation of PDGF-A expression decreases tumor incidence and increaseslatency. Thus, the tumorigenic effect of PDGF-A must act through paracrinemechanisms relevant at early stages of tumor initiation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 00:47:04