The Exceptional Responsiveness of Certain Human Myeloid Leukemia Cells to Colony-Stimulating Activity

We have studied the marrow cells from a patient with acute myeloid leukemia (AML) for their responsiveness to colony-stimulating activity (CSA) in vitro. The AML cells were stimulated by CSA to rapid and extended growth in liquid culture. In the absence of CSA, the majority of cells died. CSA also s...

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Bibliographic Details
Published in:Blood 1979-12, Vol.54 (6), p.1230-1239
Main Authors: Brennan, James K., DiPersio, John F., Abboud, Camille N., Lichtman, Marshall A.
Format: Article
Language:English
Subjects:
Adult
Bone Marrow Cells
Cell Transformation, Neoplastic
Chromatography, Gel
Clone Cells
Colony-Stimulating Factors - pharmacology
Culture Media
Giant Cell Tumors
Humans
Leukemia, Myeloid - blood
Lymphocyte Culture Test, Mixed
Male
Molecular Weight
Phytohemagglutinins - pharmacology
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Summary:We have studied the marrow cells from a patient with acute myeloid leukemia (AML) for their responsiveness to colony-stimulating activity (CSA) in vitro. The AML cells were stimulated by CSA to rapid and extended growth in liquid culture. In the absence of CSA, the majority of cells died. CSA also stimulated the clonal growth of AML cells, and the minimum requirement for CSA was one-tenth to one-fiftieth that required to stimulate the growth of normal marrow CFU-C. CSA for AML cells was eluted from Sephacryl S-200 columns in fractions that represented an apparent molecular weight of 45,000 daltons. This fraction also produced optimal stimulation of normal human marrow. During remission, the patient's marrow cells did not grow in liquid culture and produced normal numbers of granulocytic and erythroid colonies in response to CSA and erythropoietin. Extended culture of the AML cells resulted in cell differentiation evidenced by decreasing proliferative capacity and by morphological and histochemical changes. These studies indicate that certain AML cells are extraordinarily responsive to CSA, an in vitro mediator of normal granulopoiesis.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V54.6.1230.1230