ABSTRACT
I. INTRODUCTION B-cell chronic lymphocytic leukemia (B-CLL) is a unique accumulative disorder, charac terized by a low proliferative activity and by the progressive accumulation of clonal B lymphocytes blocked in the early phases (G0/G1) of the cell cycle. For a long time it had been postulated that in the pathogenesis of the disease, still largely unknown, as well as in its clinical course, an important role must be played by the dysregulation of intercellular mechanisms that normally control the progression through the cell cycle. Over the years, several altered cytokine networks have been described as capable of influencing the life span of B-CLL cells in vivo, and the neoplastic clone itself is known to produce a number of soluble factors, some of which potentially implicated in autocrine loops. Moreover, defective apoptosis (programmed cell death) and deregulation of some cell cycle regula tory genes have been shown to contribute to the malignant process in B-CLL.
