4.6 Article

Serum interleukin-17 and its relationship to angiogenic factors in multiple myeloma

Journal

EUROPEAN JOURNAL OF INTERNAL MEDICINE
Volume 17, Issue 6, Pages 412-416

Publisher

ELSEVIER
DOI: 10.1016/j.ejim.2006.02.012

Keywords

interleukin 17; multiple myeloma; angiogenesis; tumor necrosis factor-alpha; vascular endothelial-cell growth factor; microvessel density

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Background: Interleukin-17 (IL-17) is a CD4 T-cell-derived mediator of angiogenesis that stimulates vascular endothelial cell migration and regulates the production of a variety of proangiogenic factors, such as tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial cell growth factor (VEGF). Angiogenesis is implicated in the progression of multiple myeloma (MM). Methods: We measured serum levels of IL-17, TNF-alpha, and VEGF, as well as microvessel density (MVD) in 40 untreated MM patients. Results: Levels of IL-17 in the sera of patients with MM were higher than those in matched controls; however, the difference did not reach statistical significance. Serum levels of both TNF-alpha and VEGF in MM patients were significantly higher than those in controls (P<0.001 in both instances). Levels of IL-17 in MM patients, both stage 11 and stage 111, were significantly higher than those of stage I patients (p=0.001 and p<0.001, respectively). Similarly, higher values of VEGF (p<0.001), TNF-a (p<0.001), and MVD (p<0.035) were associated with advanced disease stage. Serum values of IL-17 in MM patients correlated positively not only with VEGF (Spearman's rho=0.606) and TNF-alpha (r=0.552; p<0.001 in both instances), but also with MVD (r=0.385, p=0.014). In addition, a positive correlation was found between serum values of VEGF and TNF-alpha (r=0.657, p<0.001), MVD and VEGF (r=0.353, p=0.026), and between MVD and TNF-alpha (r=0.506,p=0.001) in MM patients. Conclusion: These results suggest that IL-17 plays a role in the promotion of angiogenesis and associated disease progression in MM. (C) 2006 European Federation of Internal Medicine. Published by Elsevier B.V All rights reserved.

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