Abstract
In this paper we demonstrate that maturing neoplastic cells from patients with chronic myelogenous leukemia (CML) constitutively produce G-CSF and are also receptive for this molecule. G-CSF functions as an autocrine growth factor in stable phase CML, and thus is responsible for divisions of maturing leukemic cells leading to an expansion of the compartment of mature cells. This observation is well in line with in vivo features of CML in stable phase, i.e., the hyperplasia of the mature granulocyte compartment. In acute blastic phase of CML expression of the G-CSF gene seems to be less common and not related to autonomous blast growth.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / analysis
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Bone Marrow / pathology
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Cell Division*
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Colony-Stimulating Factors / biosynthesis
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Colony-Stimulating Factors / genetics*
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Colony-Stimulating Factors / physiology
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DNA, Neoplasm / genetics
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Granulocyte Colony-Stimulating Factor
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HLA-DR Antigens / analysis
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Humans
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology*
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Lymphocytes / immunology*
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Lymphocytes / pathology
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RNA Probes
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RNA, Messenger / analysis
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RNA, Messenger / genetics
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RNA, Neoplasm / genetics
Substances
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Antigens, CD
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Colony-Stimulating Factors
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DNA, Neoplasm
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HLA-DR Antigens
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RNA Probes
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RNA, Messenger
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RNA, Neoplasm
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Granulocyte Colony-Stimulating Factor