Conversion of Factor-Dependent Myeloid Cells to Factor Independence: Autocrine Stimulation is Not Coincident with Tumorigenicity

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Abstract
Release from normal growth requirements has long been hypothesized as an initial step in malignant progression (Holley, 1976). All cells of the myeloid lineage, from early progenitors to mature blood cells, are under the immediate control of certain growth factors that support their survival, proliferation, differentiation, and functional activation. Four of these growth factors have been characterized in in vitro culture systems for both mouse and human (for reviews see Metcalf, 1985 and Clark and Kamen, 1987). In vitro analysis of the mechanisms that may lead to disruption of the normal controls governing proliferation and differentiation is made feasible by the availability of established hematopoietic cell lines that are dependent on one or several of these factors for survival and proliferation and, in some cases, are still responsive to differentiation stimuli (Greenberger et al., 1980; Dexter et al., 1980). We present here evidence that support the hypothesis that aberrant expression of a growth factor and subsequent stimulation by an autocrine mechanism may play a pivotal role in the initial stages of malignant progression, however, tumorigenesis is not coincident with autocrine stimulation.