Format

Send to

Choose Destination
Eur J Intern Med. 2006 Oct;17(6):412-6.

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

Author information

1
Department of Haematology, University Hospital of Heraklion, P.O. Box 1352, Heraklion, Crete, Greece.

Abstract

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 II and stage III, 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-alpha (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.

PMID:
16962948
DOI:
10.1016/j.ejim.2006.02.012

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center