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Titolo:
Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein
Autore:
Scheller, M; Foerster, J; Heyworth, CM; Waring, JF; Lohler, J; Gilmore, GL; Shadduck, RK; Dexter, TM; Horak, I;
Indirizzi:
FMP, Dept Mol Genet, D-12207 Berlin, Germany FMP Berlin Germany D-12207FMP, Dept Mol Genet, D-12207 Berlin, Germany Free Univ Berlin, Klinikum Benjamin Franklin, D-12200 Berlin, Germany FreeUniv Berlin Berlin Germany D-12200 ranklin, D-12200 Berlin, Germany Univ Hamburg, Heinrich Pette Inst Expt Virol & Immunol, D-2000 Hamburg, Germany Univ Hamburg Hamburg Germany D-2000 l & Immunol, D-2000 Hamburg, Germany Paterson Inst Canc Res, Manchester M20 9BX, Lancs, England Paterson Inst Canc Res Manchester Lancs England M20 9BX X, Lancs, England Western Penn Canc Inst, Pittsburgh, PA USA Western Penn Canc Inst Pittsburgh PA USA n Canc Inst, Pittsburgh, PA USA
Titolo Testata:
BLOOD
fascicolo: 11, volume: 94, anno: 1999,
pagine: 3764 - 3771
SICI:
0006-4971(199912)94:11<3764:ADACRO>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC MYELOGENOUS LEUKEMIA; COLONY-STIMULATING FACTOR; REGULATORY FACTOR FAMILY; STEM-CELL FACTOR; PHILADELPHIA-CHROMOSOME; FACTOR-I; DIFFERENTIATION; PROLIFERATION; FIBRONECTIN; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Horak, I FMP, Dept Mol Genet, Krahmerstr 6, D-12207 Berlin, Germany FMP Krahmerstr 6 Berlin Germany D-12207 D-12207 Berlin, Germany
Citazione:
M. Scheller et al., "Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein", BLOOD, 94(11), 1999, pp. 3764-3771

Abstract

Mice deficient for the transcription factor, interferon consensus sequencebinding protein (ICSBP), are immunodeficient and develop disease symptoms similar to human chronic myeloid leukemia (CML). To elucidate the hematopoietic disorder of ICSBP-/- mice, we investigated the growth, differentiation, and leukemogenic potential of ICSBP-/- myeloid progenitor cells in vitro,as well as by cell-transfers in vivo. We report that adult bone marrow, aswell as fetal liver of ICSBP-deficient mice harbor increased numbers of progenitor cells, which are hyperresponsive to both granulocyte macrophage colony-stimulating factor (GM-CSF) and G-CSF in vitro, In contrast, their response to M-CSF is strongly reduced and, surprisingly, ICSBP-/- colonies formed in the presence of M-CSF are mostly of granulocytic morphology. This disproportional differentiation toward cells of the granulocytic lineage in vitro parallels the expansion of granulocytes in ICSBP-/- mice and correlates with a 4-fold reduction of M-CSF receptor expressing cells in bone marrow. Cell transfer studies showed an intrinsic leukemogenic potential and long-term reconstitution capability of ICSBP-/- progenitors. Further experiments demonstrated strongly reduced adhesion of colony-forming cells from ICSBP-/- bone marrow to fibronectin. In summary, ICSEP-/- myeloid progenitor cells share several abnormal features with CML progenitors, suggesting that the distal parts of signaling pathways of these two disorders are overlapping. (C) 1999 by The American Society of Hematology.

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Documento generato il 28/11/20 alle ore 15:16:49