B-cell chronic lymphocytic leukaemia (B-CLL) is a clinically heterogeneous disease characterised by the accumulation of a clonal population of B lymphocytes. This accumulation is considered to result from the prolonged survival of B-CLL cells arrested in the G0 stage of the cell cycle. However, when cultured in vitro, B-CLL cells die rapidly by apoptosis. It is now clear that a number of factors can delay or postpone the onset of apoptosis, including a number of cytokines and direct contact with different cell types. Although many drugs are now known to cause clinical improvement in B-CLL by causing apoptosis of B-CLL cells, in only a few cases have biological mechanisms been reported to have similar effects. It is now important to understand the role of these mechanisms in the pathogenesis and progression of B-CLL, and to devise strategies to exploit them for therapeutic use
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