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Advances in Hematology
Volume 2009, Article ID 287974, 6 pages
http://dx.doi.org/10.1155/2009/287974
Research Article

Does Adiponectin Act as an Antiangiogenic Factor in B-Cell Chronic Lymphocytic Leukemia?

1Medical Oncology Unit, Department of Hematology-Oncology, Azienda Ospedaliera Pugliese-Ciaccio, 88100 Catanzaro, Italy
2Department of Clinical Pathology, IRCCS Regina Elena, Roma, Italy
3Department of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy
4Laboratorio di Genetica Molecolare, IRCCS Policlinico, Milano, Italy
5Department of Hematology, Azienda Ospedaliera Verona, Cosenza, Italy
6Department of Human Anatomy and Histology, University of Bari Medical School, Bari, Italy

Received 18 May 2009; Accepted 21 May 2009

Academic Editor: Maher Albitar

Copyright © 2009 Stefano Molica et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Angiogenesis is involved in the pathogenesis of B-cell chronic lymphocytic leukemia (CLL), and high microvascular density has been found in CLL to be associated with a poor prognosis. In this study, we assessed serum levels of adiponectin in 69 patients with Binet stage A B-CLL, and these values were retrospectively correlated with bone marrow (BM) microvessel area and serum levels of vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), angiogenin, PECAM-1 (CD31), matrix metalloproteinase-9 (MMP-9), interleukin-8 (IL-8), syndecan-1, and the percentage of or CLL cells. The positive correlation between serum levels of adiponectin and VEGF ( ) does not translate into an increase of the extent of BM angiogenesis ( ), FGF-2 ( ), angiogenin ( ), and CD31 ( ) serum concentrations. Accordingly, IL-8 ( ), syndecan-1 ( ), and MMP-9 ( ) circulating levels were not likely to reflect adiponectin concentration. Furthermore, patients with higher levels of adiponectin had a more favorable biological profile as defined by a lower number of both ( ; ) and ( ; ). Finally, we evaluated the presence of adiponectin in B-CLL cells at gene expression level. RMA intensity values for adiponectin gene transcript denote a homogeneous low expression in B-CLL cells, whereas VEGF transcript was highly expressed with a degree of interpatient variability. Overall, these data seem to indicate that adiponectin could be involved as an antiangiogenic factor in B-CLL.