Download Chronic Lymphocytic Leukemia (Current Topics in Microbiology by by Federico Caligaris-Cappio (Editor), Riccardo Dalla Favera PDF
By by Federico Caligaris-Cappio (Editor), Riccardo Dalla Favera (Editor)
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Extra info for Chronic Lymphocytic Leukemia (Current Topics in Microbiology and Immunology)
Perhaps B-CLL and HCL are commonly derived from the malignant transformation of a similar cellular precursor, a CD27+ marginal zone or a memory B cell (Fig. 1). The different transformation processes acting on the precursor cells would determine their distinct phenotype and clinical presentation. Alternatively, the two tumor entities could be derived from the malignant transformation of distinct subsets of CD27+ B cells (see previous section). In fact, a possible relationship between HCL and a particular tonsillar, somatically mutated B cell subpopulation (phab V-3+ , CD27+ , CD11c+ , CD23− ) has been noted (van Der Vuurst De Vries and Logtenberg 1999; Basso et al.
2000; Jelinek et al. 2001; Hamblin et al. 2002), in part due to the fact that CD38 expression levels are heterogeneous within the same tumor case and may also change over New Insights into the Phenotype and Cell Derivation of B Cell 33 the disease course (Hamblin et al. 2002). Third, IgV gene repertoire analyses early on suggested that B-CLL express a restricted set of IgV gene segments (Chiorazzi and Ferrarini 2003), a circumstance that invokes a possible role for antigen in the pathogenesis of B-CLL.
First, MyD118 (expressed in small pre-BII cells) and EAT/MCL-1 (expressed from immature B cells onwards) could inactivate proliferating-cell nuclear antigen (PCNA; a major cell-cycle regulator expressed in pre-BI and large pre-BII cells) by heterodimerization. Second, cdc25 is phosphorylated by the DNAdamage inducible kinase chk-1, which generates a 14-3-3 binding site. Binding of 14-3-3, expressed in small pre-BII cells, to cdc25, in turn, renders cdc25 inactive, blocking cell-cycle progression.