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Titolo:
Defective regulation of leukemic hematopoiesis in chronic myeloid leukemia
Autore:
Eaves, C; Cashman, J; Eaves, A;
Indirizzi:
BC Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada BC Canc Agcy Vancouver BC Canada V5Z 1L3 b, Vancouver, 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 Univ British Columbia, Dept Med Pathol, Vancouver, BC V5Z 1L3, Canada UnivBritish Columbia Vancouver BC Canada V5Z 1L3 ver, BC V5Z 1L3, Canada Univ British Columbia, Dept Lab Med, Vancouver, BC V5Z 1L3, Canada Univ British Columbia Vancouver BC Canada V5Z 1L3 ver, BC V5Z 1L3, Canada
Titolo Testata:
LEUKEMIA RESEARCH
fascicolo: 12, volume: 22, anno: 1998,
pagine: 1085 - 1096
SICI:
0145-2126(199812)22:12<1085:DROLHI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC MYELOGENOUS LEUKEMIA; GROWTH-FACTOR-BETA; HUMAN-BONE-MARROW; COLONY-STIMULATING FACTOR; LONG-TERM HEMATOPOIESIS; EXPANSION IN-VITRO; STEM-CELLS; PROGENITOR CELLS; COMMITTED PROGENITORS; TARGETED DISRUPTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
86
Recensione:
Indirizzi per estratti:
Indirizzo: Eaves, C BC Canc Agcy, Terry Fox Lab, 601 W 10th Ave, Vancouver, BC V5Z 1L3, Canada BC Canc Agcy 601 W 10th Ave Vancouver BC Canada V5Z 1L3 3, Canada
Citazione:
C. Eaves et al., "Defective regulation of leukemic hematopoiesis in chronic myeloid leukemia", LEUK RES, 22(12), 1998, pp. 1085-1096

Abstract

Over the last two decades considerable knowledge has been acquired about the distribution of cell types within the dominant leukemic (Ph+/BCR-ABL(+))clone that results in human chronic myeloid leukemia (CML). Evidence is now growing to indicate that three key biological changes affecting the development of such clones are: (1) an increased probability of differentiation at the level of the most primitive leukemic stem cells, (2) an increased turnover rate of the leukemic progenitors at all stages of differentiation; and (3) their increased ability to survive under conditions of factor-deprivation. Such a model explains the long latent period for the development of CML as well as why normal stem cells may persist in large numbers but stillfail to compete in contributing to the daily output of mature blood cells in patients with disease. The recent development of new genetic and transplant models of human CMI. may now allow thr molecular basis of these biological disturbances to be delineated and more effective therapeutic strategiesdeveloped. (C) 1998 Elsevier Science Ltd. Ail rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 00:29:18