By Hartmut Beug, Peter Steinlein, Petr Bartunek, and Michael J. Hayman
Hematopoietic cells are produced throughout the lifetime of an individual from a small set of stem cells. The progeny of these stem cells make decisions involving self-renewal and differentiation to give rise to the cells of the erythroid, myeloid, and lymphoid lineages.1 These cells either proliferate, to expand a certain compartment, or differentiate along a lineage-specific pathway. Through a delicate balance between proliferation and differentiation, the numbers of the cells within various lineages are controlled and homeostasis is maintained. A crucial role in this process is played by cytokines, which regulate the proliferation and differentiation of progenitors as well as the function of mature cells.2-3
Leukemias and lymphomas are diseases in which the delicate equilibrium between proliferation and differentiation has been disturbed. This results in dramatic changes in the phenotypic spectrum of hematopoietic cells found in the body, usually characterized by the hyperproliferation of immature or partially mature hematopoietic cells at the expense of mature, functional ones.3 In order to understand the mechanisms underlying these
1 J. E. Till and E. A. McCulloch, Biochim. Biophys. Acta 605, 431 (1980).
1 C. L. Sawyers, C. T. Denny, and O. N. Witte, Cell (Cambridge, Mass.) 64, 337 (1991).
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