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Abolished angiogenicity and tumorigenicity of Burkitt lymphoma by interleukin-10

Author:
  • L Cervenak
  • L Morbidelli
  • D Donati
  • S Donnini
  • T Kambayashi
  • J L Wilson
  • H Axelson
  • E Castaños-Velez
  • H G Ljunggren
  • R D Malefyt
  • H J Granger
  • M Ziche
  • M T Bejarano
Publishing year: 2000-10-01
Language: English
Pages: 73-2568
Publication/Series: Blood
Volume: 96
Issue: 7
Document type: Journal article
Publisher: American Society of Hematology

Abstract english

Because of its immunosuppressive properties, interleukin-10 (IL-10) is thought to play an important role in a number of human disease states, including inflammation, autoimmunity, and transplant rejection. In this study, we demonstrate that introduction of human or viral IL-10 genes into Burkitt's lymphoma cells markedly reduced their ability to grow as subcutaneous (sc) tumors in SCID mice. In vivo assays for angiogenesis revealed an inhibition of the angiogenic capacity of the IL-10-transfected lines. Recombinant human IL-10 abolished and viral IL-10 reduced vascular endothelial growth factor (VEGF)-165-induced neovascularization. Furthermore, IL-10 blocked the VEGF- and fibroblast growth factor (FGF)-2-induced proliferation of microvascular endothelial cells in vitro. The current observations suggest a direct role for IL-10 in the prevention of angiogenesis in human lymphoid malignancies.

Keywords

  • Cancer and Oncology
  • Animals
  • Burkitt Lymphoma
  • Cell Division
  • Cell Line
  • Endothelial Growth Factors
  • Endothelium, Vascular
  • Fibroblast Growth Factor 2
  • Gene Expression
  • Interleukin-10
  • Killer Cells, Natural
  • Lymphokines
  • Mice
  • Mice, SCID
  • Neoplasm Transplantation
  • Neovascularization, Pathologic
  • Rabbits
  • Recombinant Proteins
  • Transfection
  • Tumor Cells, Cultured
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Other

Published
  • ISSN: 0006-4971
Håkan Axelson
E-mail: hakan.axelson [at] med.lu.se

Professor

Division of Translational Cancer Research

+46 46 222 64 34

MV 404 A31A2

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