Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Autocrine production and action of IL-3 and granulocyte colony-stimulatingfactor in chronic myeloid leukemia
Autore:
Jiang, XY; Lopez, A; Holyoake, T; Eaves, A; Eaves, C;
Indirizzi:
British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada British Columbia Canc Agcy Vancouver BC Canada V5Z 1L3 BC V5Z 1L3, Canada Hanson Ctr Canc Res, Adelaide, SA, Australia Hanson Ctr Canc Res AdelaideSA Australia c Res, Adelaide, SA, Australia Univ British Columbia, Dept Med, Vancouver, BC V5Z 1L3, Canada Univ British Columbia Vancouver BC Canada V5Z 1L3 ver, BC V5Z 1L3, Canada Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1L3, Canada Univ British Columbia Vancouver BC Canada V5Z 1L3 ver, BC V5Z 1L3, Canada Univ British Columbia, Dept Med Genet, Vancouver, BC V5Z 1L3, Canada Univ British Columbia Vancouver BC Canada V5Z 1L3 ver, BC V5Z 1L3, Canada
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 22, volume: 96, anno: 1999,
pagine: 12804 - 12809
SICI:
0027-8424(19991026)96:22<12804:APAAOI>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC MYELOGENOUS LEUKEMIA; TYROSINE KINASE-ACTIVITY; BCR-ABL ONCOGENE; HUMAN HEMATOPOIETIC-CELLS; CONSTITUTIVE ACTIVATION; PROGENITOR CELLS; NOD/SCID MICE; CD34(+) CELLS; CHRONIC-PHASE; INTERLEUKIN-3;
Keywords:
stem cells; growth factors; STAT5;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Eaves, C British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3,Canada British Columbia Canc Agcy Vancouver BC Canada V5Z 1L3 3, Canada
Citazione:
X.Y. Jiang et al., "Autocrine production and action of IL-3 and granulocyte colony-stimulatingfactor in chronic myeloid leukemia", P NAS US, 96(22), 1999, pp. 12804-12809

Abstract

Primitive subsets of leukemic cells isolated by using fluorescence-activated cell sorting from patients with newly diagnosed Ph+/BCR-ABL(+) chronic myeloid leukemia display an abnormal ability to proliferate in vitro in the absence of added growth factors. We now show from analyses of growth-factorgene expression, protein production, and antibody inhibition studies that this deregulated growth can be explained, at least in part, by a novel differentiation-controlled autocrine mechanism. This mechanism involves the consistent and selective activation of IL-3 and granulocyte colony-stimulatingfactor (G-CSF) production and a stimulation of STAT5 phosphorylation in CD34(+) leukemic cells. When these cells differentiate into CD34(-) cells in vivo, IL-3 and C-CSF production declines, and the cells concomitantly lose their capacity for autonomous growth in vitro despite their continued expression of BCR-ABL Based on previous studies of normal cells, excessive exposure of the most primitive chronic myeloid leukemia cells to IL-3 and G-CSF through an autocrine mechanism could explain their paradoxically decreased self-renewal in vitro and slow accumulation in vivo, in spite of an increased cycling activity and selective expansion of later compartments.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 22:13:15