The pathogenesis of B-cell chronic lymphocytic leukemia (CLL) and the mechanisms regulating the growth, survival, and expansion of the leukemic clone are still largely unknown, but there is growing evidence of the important role played by cytokine networks and soluble mediators in the leukemic process. Leukemic CLL cells represent the most prominent population in CLL, but not the only one. Accessory non-neoplastic hematopoietic cells circulate in the peripheral blood and bone marrow of CLL patients, and cells of stromal origin are in strict contact with the tumor clone. The crosstalk between all these cell populations is mediated by soluble factors that may influence the pattern of survival and expansion of the disease, as well as the function of the normal compartment. The peculiar and in many ways unique clinical picture of CLL is likely to arise from the complex interactions of different networks, in which the action of one cytokine may strongly influence the production of, and response to, another. In the present chapter we discuss the role that different cytokines and soluble molecules may play, alone or through complex interactions, both on the leukemic clone and on the clinical course of the disease. For the sake of clarity, we discuss separately cytokines that induce cell survival, inhibitory cytokines, and soluble molecules.

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