作者: Julien Bouley , Ludovic Deriano , Jozo Delic , Hélène Merle-Béral
DOI: 10.1080/10428190500513835
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摘要: B-chronic lymphocytic leukemia (B-CLL) is characterized by a highly variable clinical course which has long remained stumbling block for clinicians. This variability appears to arise from complex molecular alterations identified in malignant cells patient subsets. Recent studies have focused particular on identifying new markers help predict the most effective and adapted treatments. In addition mutation status of immunoglobulin heavy-chain region (IgVH) genes, well-established predictive factor B-CLL, these include defects cell factors involved maintenance genome stability, such as telomere function, DNA repair, ATM p53. Other factors, tyrosine kinase Zap-70 soluble found sera, may be associated with B-cell receptor signal transduction. Interestingly, an alteration fits closely, though not strikingly, absence somatic mutations IgVH suggesting that latter due either epigenetic events leading unstable or inherited defect immune response B-cells. lessons expression/phosphorylation suggest some reflect defective pathways B-CLL rather than being malignancy per se. Furthermore, specific subsets are resistant treatment. Current gene expression profiling proteomic analyses should soon lead better understanding how affected, especially multi-drug B-CLL.