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Titolo:
Excessive apoptosis in low risk myelodysplastic syndromes (MDS)
Autore:
Parker, JE; Mufti, GJ;
Indirizzi:
Guys Kings Thomas Sch Med, Dept Haematol Med, London SE5 8RX, England GuysKings Thomas Sch Med London England SE5 8RX London SE5 8RX, England
Titolo Testata:
LEUKEMIA & LYMPHOMA
fascicolo: 1-2, volume: 40, anno: 2000,
pagine: 1 - 24
SICI:
1042-8194(200012)40:1-2<1:EAILRM>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; RECOMBINANT-HUMAN-ERYTHROPOIETIN; COLONY-STIMULATING FACTOR; FLOW CYTOMETRIC DETECTION; REGULATES FAS/TNFR1-INDUCED APOPTOSIS; DEPENDENT KINASE INHIBITORS; CYTOTOXIC LIGAND TRAIL; CELL-CYCLE PROGRESSION; SEVERE APLASTIC-ANEMIA; CYTOCHROME-C RELEASE;
Keywords:
MDS; apoptosis; fas; TNF-alpha bel-2;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
199
Recensione:
Indirizzi per estratti:
Indirizzo: Mufti, GJ Guys Kings Thomas Sch Med, Dept Haematol Med, Denmark Hill Campus, London SE5 8RX, England Guys Kings Thomas Sch Med Denmark Hill Campus London England SE5 8RX
Citazione:
J.E. Parker e G.J. Mufti, "Excessive apoptosis in low risk myelodysplastic syndromes (MDS)", LEUK LYMPH, 40(1-2), 2000, pp. 1-24

Abstract

The paradox of peripheral cytopenias despite a normo/hypercellular marrow in MDS has been ascribed to excessive intramedullary hematopoietic cell apoptosis. Programmed cell death (PCD) in early disease might be triggered by the BM microenvironment, mediated either through inhibitory cytokines such as tumor necrosis factor alpha (TNF-alpha) or fas/fas ligand signaling or through a relative deficiency in hematopoietic growth factors. Intrinsic cellular defects giving rise to abnormalities in cell-cell or cell-stromal interaction, cell signaling or cell cycling may also underlie hematopoietic progenitor apoptosis. Alternatively, an early 'hit' in the multistep pathogenesis of MDS may result in a higher proliferative rate of the neoplastic clone. Increased apoptosis may thus represent a homeostatic process to controlcell numbers. This paper shall summarize current evidence implicating a role for increased PCD in low risk MDS, outline possible etiologic factors and suggest potential therapeutic mechanisms whereby excessive hematopoietic progenitor cell apoptosis might he circumvented.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 06:32:50