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Details for article 5 of 5 found articles
| Title: |
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 |
| Author: |
Trojani, Alessandra Di Camillo, Barbara Tedeschi, Alessandra Lodola, Milena Montesano, Simona Ricci, Francesca Vismara, Eleonora Greco, Antonino Veronese, Silvio Orlacchio, Aldo Martino, Sabata Colombo, Chiara Mura, Mariangela Nichelatti, Michele Colosimo, Anna Scarpati, Barbara Montillo, Marco Morra, Enrica |
| Appeared in: |
Disease markers. Section A, Cancer biomarkers |
| Paging: | Volume 11 (2012) nr. 1 pages 15-28 |
| Year: |
2012-07-19 |
| Contents: |
Background: 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. Design and methods: 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^{+}. Results: 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. Conclusions: 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. |
| Publisher: |
IOS Press |
| Source file: |
Elektronische Wetenschappelijke Tijdschriften |
Details for article 5 of 5 found articles
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