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RESEARCH PRODUCT

Mechanisms of Autocrine and Paracrine Growth Control in Acute Myelogenous Leukemia

subject

description

Blast cells of a high proportion of patients with acute myelogenous leukemia (AML) proliferate in response to exogenous hematopoetic growth factors, both in vitro [9, 14, 26, 36, 48, 65] and in vivo [20]. Whereas leukemic colony-forming cells (L-CFCs) from most patients share their growth factor dependence with normal committed myeloid progenitor cells (CFU-GMs), some AML samples autonomously form colonies in agar and are therefore believed to bypass growth factor requirements [17, 42, 72]. Autocrine growth factor production has been identified as one mechanism used by AML blasts to supply various growth-promoting molecules. Moreover nontransformed accessory bone marrow cells have been shown to be inducible for production of growth-promoting factors by AML-derived mediators. This paper summarizes the current knowledge of autocrine and paracrine growth-promoting mechanisms in AML whereby leukemic cells may achieve selective growth advantages and includes recent data supporting the concept that various cytokines may act in concert to induce optimal leukemic growth.