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粒细胞-巨噬细胞集落刺激因子基因在急性髓细胞白血病中的组成性表达。

Constitutive expression of the granulocyte-macrophage colony-stimulating factor gene in acute myeloblastic leukemia.

作者信息

Young D C, Wagner K, Griffin J D

出版信息

J Clin Invest. 1987 Jan;79(1):100-6. doi: 10.1172/JCI112769.

DOI:10.1172/JCI112769
PMID:3491836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC423997/
Abstract

Expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) gene was studied by Northern blot analysis in normal human hematopoietic cells and a series of leukemias. GM-CSF messenger (m)RNA was detected in activated T cells, but not in normal bone marrow cells, monocytes, or nonactivated T cells. In contrast, leukemic cells from 11 of 22 cases of acute myeloblastic leukemia expressed GM-CSF transcripts. Biologically active CSF was detected in supernatant conditioned by 6 of these 11 leukemias. Expression of the GM-CSF gene was not detected in "common" (pre-B cell) acute lymphoblastic leukemia (11 cases tested) or chronic myeloid leukemia (4 cases tested). These results show that the GM-CSF gene is constitutively expressed in a subset of patients with AML, and further suggest that expression of this gene could contribute to the abnormal growth properties characteristic of AML.

摘要

采用Northern印迹分析法,对正常人造血细胞及一系列白血病细胞中粒细胞-巨噬细胞集落刺激因子(GM-CSF)基因的表达进行了研究。在活化的T细胞中检测到GM-CSF信使核糖核酸(mRNA),但在正常骨髓细胞、单核细胞或未活化的T细胞中未检测到。相反,22例急性髓细胞白血病中有11例的白血病细胞表达GM-CSF转录本。在这11例白血病中的6例所产生的上清液中检测到了具有生物学活性的集落刺激因子(CSF)。在“普通”(前B细胞)急性淋巴细胞白血病(检测11例)或慢性髓细胞白血病(检测4例)中未检测到GM-CSF基因的表达。这些结果表明,GM-CSF基因在一部分急性髓细胞白血病患者中组成性表达,进一步提示该基因的表达可能促成了急性髓细胞白血病特有的异常生长特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e057/423997/23648da647fd/jcinvest00112-0114-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e057/423997/86b26fb28b01/jcinvest00112-0114-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e057/423997/23648da647fd/jcinvest00112-0114-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e057/423997/86b26fb28b01/jcinvest00112-0114-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e057/423997/23648da647fd/jcinvest00112-0114-b.jpg

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