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      Gene expression profiling identifies ARSD as a new marker of disease progression and the sphingolipid metabolism as a potential novel metabolism in chronic lymphocytic leukemia.

      Cancer biomarkers : section A of Disease markers
      Adult, Aged, Arylsulfatases, genetics, metabolism, Cluster Analysis, Disease Progression, Female, Genes, Humans, Immunoglobulin Heavy Chains, Kaplan-Meier Estimate, Leukemia, Lymphocytic, Chronic, B-Cell, enzymology, mortality, pathology, Logistic Models, Male, Middle Aged, Multivariate Analysis, Oligonucleotide Array Sequence Analysis, Prognosis, Proportional Hazards Models, Sphingolipids, Transcriptome, Tumor Markers, Biological, ZAP-70 Protein-Tyrosine Kinase

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          Abstract

          Several studies demonstrated IGVH mutational status and ZAP70 expression as the most relevant prognostic markers in Chronic Lymphocytic Leukemia (CLL), suggesting the separation of two patient subgroups: with good mutated ZAP70 negative (MTZAP70(-) and poor unmutated ZAP70 positive (UMZAP70(+)) prognosis. We determined the gene expression of B cells in 112 CLL patients divided into three classes: class 1 with MTZAP70(-), class 2 with UMZAP70(+), and class 3 included both UMZAP70(-) and MTZAP70(+). We found LPL, AGPAT2, MBOAT1, CHPT1, AGPAT4, PLD1 genes encoding enzymes involved in lipid metabolism overexpressed in UMZAP70(+). In addition, this study identified ARSD, a gene belonging to the sphingolipid metabolism, as a new gene significantly overexpressed in UMZAP70(+) compared to MTZAP70(-). Western blots confirmed that ARSD protein levels were significantly different between the 3 classes of patients and normal controls. Statistical analysis identified a significant correlation between ARSD and IGVH; however, both ARSD protein level and IGVH were independently associated with the need for therapy of CLL patients. ARSD is a novel prognostic factor as the time to start therapy is shorter in patients with high levels of ARSD protein and sphingolipid metabolism could represent a new biological mechanism in CLL.

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