By P. Oppezzo
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However this traditional view that CLL is a disease deriving from an inherent defect in apoptosis has being called into question . Recent studies suggest that CLL is a dynamic process, comprising leukemic cells that multiply and die at measurable rates. Furthermore, since CLL cells do not appear to be inherently immortal, patient´s compromise does not occur from passive accumulation, but from active generation of subclones that over time develop dangerous genetic abnormalities which further change the birth/death ratios [10,11].
1999) Bryostatin and CD40-ligand enhance apoptosis resistance and induce expression of cell survival genes in B-cell chronic lymphocytic leukaemia. A. J. (1993) Activated T cells induce expression of B7/BB1 on normal or leukemic B cells through a CD40-dependent signal. J Exp Med 177 (4), 925-935  Lagneaux, L. et al. (1998) Chronic lymphocytic leukemic B cells but not normal B cells are rescued from apoptosis by contact with normal bone marrow stromal cells. Blood 91 (7), 2387-2396  Vaisitti, T.
The interest has been initially focused upon Microenvironment Interactions in Chronic Lymphocytic Leukemia: A Delicate Equilibrium Linking the Quiescent and the Proliferative Pool 25 adhesion molecules. In-vitro, it has been shown that malignant CLL B-cells interact with BM stromal cells via β1 and β2 integrins . This binding rescues CLL cells from apoptosis and extends their lifespan, suggesting a potential mechanism for the preferential in-vivo accumulation and survival of CLL cells within the BM.