Abstract
It has been shown that cells from normal human bone marrow are capable of forming granulocytic colonies in vitro in the presence of an appropriate granulopoietic stimulus (1-3). Under similar conditions blast cells from the peripheral blood and bone marrow of patients with acute granulocytic leukemia (AGL) form granulocytic colonies which are morphologically similar to those of normal bone marrow but are smaller in size (4-7). The reasons for the small colony size are unclear. The possibilities that have been suggested are: (a) A decreased production of granulopoietic substances in AGL (8), (b) a basic defect in granulocyte precursor cells in AGL making them insensitive to the biologic effects of granulopoietic substances (9), or (c) the presence of inhibitory substances preventing granulopoietic factors from acting on these cells (10).
The first suggestion is unlikely in view of our findings of normal levels of granulopoietic substances, as measured by the colony stimulating activity (CSA) of serum and urine in patients with AGL during remission (8, 9). The possibility of inhibitory substances is also not likely in view of our recent work (10) and that of others (11). It has been shown in our own studies that serum and plasma from patients with AGL during the relapse phase of their disease do not inhibit the colony growth of normal human bone marrow cells (10).
It seems reasonable to suggest that the poor colony growth seen with leukemic cells is the result of a basic defect rendering them less responsive to stimulating factors. Addition of cortisone, bacteria, bacterial products, alphamethylglucoparanoside, or tryp-sinization of cell coats has not produced increased colony growth of either normal or leukemic cells in our laboratory.
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