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Abnormal erythropoiesis in the myeloproliferative disorders: an analysis of underlying cellular and humoral mechanisms.

作者信息

Eaves A C, Henkelman D H, Eaves C J

出版信息

Exp Hematol. 1980;8 Suppl 8:235-47.

PMID:6962070
Abstract

Peripheral blood and bone marrow specimens from patients with polycythemia vera (PV) and chronic myelogenous leukemia (CML) were assayed for erythroid and granulopoietic progenitor cells. All compartments were increased in CML patients in relapse although the ratio of BFU-E to CFU-C numbers remained constant in all CML patients where values ranged over several orders of magnitude. By comparison with normal ratios there was only a slight shift towards increased CFU-C numbers. No quantitative changes in any progenitor compartment was found in PV except for a marginal increase in marrow CFU-E. Erythropoietin (epo)-independent colony formation has been documented in all 61 cases of PV studied to date, and the proportion of progenitors classified as abnormal on this basis increases on average 3- to 5-fold as they differentiate in vivo from primitive BFU-E to CFU-E. Preliminary replating studies suggest that when this occurs in vitro individual BFU-E produce both normal and abnormal phenotypes. Epo-independent erythropoiesis has also been commonly observed in assays of CML cells, although its expression is more variable and in the absence of epo progenitors in CML usually make fewer erythroblasts containing even less hemoglobin than do their counterparts in PV. Expression of a common regulatory defect in erythroid cells in PV and CML suggests a possible relationship to the initial transformation event(s).

摘要

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引用本文的文献

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2
Erythroid colony growth from peripheral blood and bone marrow in polycythaemia.真性红细胞增多症患者外周血和骨髓中红系集落生长情况
J Clin Pathol. 1990 Nov;43(11):937-41. doi: 10.1136/jcp.43.11.937.
3
Rapid decline of chronic myeloid leukemic cells in long-term culture due to a defect at the leukemic stem cell level.由于白血病干细胞水平的缺陷,长期培养的慢性髓性白血病细胞迅速减少。
Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6192-6. doi: 10.1073/pnas.89.13.6192.