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Therefore, understanding the crosstalk between malignant B-cells and their milieu could give us new keys in the cellular and molecular biology of CLL that can finally lead to novel strategies in the treatment of this disease. 7. References [1] Dighiero, G. J. (2008) Chronic lymphocytic leukaemia. Lancet 371 (9617), 1017-1029 [2] Dighiero, G. (2003) Unsolved issues in CLL biology and management. Leukemia 17 (12), 2385-2391 34 Chronic Lymphocytic Leukemia [3] Vasconcelos, Y. et al. (2003) Binet's staging system and VH genes are independent but complementary prognostic indicators in chronic lymphocytic leukemia.

Cycles of these last two events overtime, produce an increase in the number of proliferating AIDpos CLL B-cells (detectable in peripheral blood), which is considered as a hallmark of a proliferative and progressive leukemia. 5. Inflammation role in an activated CLL microenvironment The relationship between antigen stimulation/inflammation and the natural history of CLL is not surprising considering that inflammation is involved in the initiation and progression of several chronic lymphoid malignancies of B-cell type [59].

A. (2010) Chemokines and chemokine receptors in chronic lymphocytic leukemia (CLL): from understanding the basics towards therapeutic targeting. Semin Cancer Biol 20 (6), 424-430 [18] Schulz, A. et al. (2010) Inflammatory cytokines and signaling pathways are associated with survival of primary chronic lymphocytic leukemia cells in vitro: a dominant role of CCL2. Haematologica [19] Zucchetto, A. et al. (2009) CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphocytic leukemia cell survival.

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