Vascular endothelial growth factor receptor-3 expression in mycosis fungoides. Issue 4 (April 2013)

• Record Type: Journal Article
• Authors: Pedersen, Ida Holst; Willerslev-Olsen, Andreas; Vetter-Kauczok, Claudia; Krejsgaard, Thorbjørn; Lauenborg, Britt; Kopp, Katharina Luise; Geisler, Carsten; Bonefeld, Charlotte M.; Zhang, Qian; Wasik, Mariusz A.; Dabelsteen, Sally; Woetmann, Anders; Becker, Jurgen C.; Odum, Niels
• Is Part Of: Leukemia & lymphoma. Volume 54:Issue 4(2013:Apr.)
• Page Start: 819
• Page End: 826
• Publication Date: 2013-04
• Subjects: Leukemia -- Periodicals; Lymphomas -- Periodicals; 616.99419
• DOI: 10.3109/10428194.2012.726720
• Languages: English
• ISSNs: 1042-8194

Abstract

<abstract> <title>Abstract</title> <p>Here, we have studied vascular endothelial growth factor receptor-3 (VEGFR-3) expression in mycosis fungoides (MF), the most common type of cutaneous T-cell lymphoma (CTCL). Immunohistochemistry revealed that in two-thirds of 34 patients, VEGFR-3 was expressed <italic>in situ</italic> by both tumor and stromal cells irrespective of the disease stage. The natural VEGFR-3 ligand, VEGF-C, partially protected malignant T-cell lines from growth inhibition by the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA). Whereas the malignant T cells did not produce VEGF-C <italic>in vitro</italic>, its expression was induced during tumor formation <italic>in vivo</italic> in a xenograft mouse model of MF. In conclusion, malignant and stromal cells express high levels of VEGFR-3 in all stages of MF. Moreover, malignant T cells trigger enhanced VEGF-C expression in fibroblasts, suggesting that cross-talk between tumor and stromal cells plays a role in lymphangiogenesis and possibly disease progression.</p> </abstract>