Misc.

Mar, 2009

Angiogenic mediators of the angiopoietin system are highly expressed by CD10-positive lymphoma cells in angioimmunoblastic T-cell lymphoma

BRITISH JOURNAL OF HAEMATOLOGY
  • Klio Konstantinou
  • Kouhei Yamamoto
  • Fumiaki Ishibashi
  • Yuiko Mizoguchi
  • Morito Kurata
  • Yasunori Nakagawa
  • Kenshi Suzuki
  • Motoji Sawabe
  • Masatsugu Ohta
  • Shigesaburo Miyakoshi
  • James T. Crawley
  • Masanobu Kitagawa
  • Display all

Volume
144
Number
5
First page
696
Last page
704
Language
English
Publishing type
DOI
10.1111/j.1365-2141.2008.07534.x
Publisher
WILEY-BLACKWELL PUBLISHING, INC

Angioimmunoblastic T-cell lymphoma (AILT) is a malignant disease of peripheral T-cell origin that is characterized by a prominent proliferation of high endothelial venules in the lymph node. To investigate angiogenic mechanisms in AILT we measured the angiogenic mediator gene expression levels in the lymph nodes of 54 non-Hodgkin lymphoma patients, by immunostaining and quantitative reverse transcription polymerase chain reaction. Angiogenic mediators angiopoietin (Ang) 1 (ANGPT1), Ang2 (ANGPT2) and their receptor, Tie2 (TEK), vascular endothelial growth factor (VEGF; VEGFA) and its receptor, VEGFR2 (KDR), and hepatocyte growth factor (HGF) and its receptor, c-Met (MET) were all more highly expressed in AILT lymph nodes (16 cases) than in B-cell lymphomas (24 cases). Moreover, significantly higher Ang1 and Tie2 expression was detected in AILT cases with CD10-positive neoplastic T-cells by comparison with unspecified peripheral T-cell lymphoma (14 cases). Immunostaining confirmed the expression of Ang1 and VEGF by both neoplastic T-cells and follicular dendritic cells. These results suggest that the angiopoietin system may play an important role in the development of high vascularity in AILT lymph nodes. Consequently, as neoplastic T-cells and follicular dendritic cells are both increased in AILT and may represent an important source of angiogenic mediators, targeting these cells with anti-angiogenic strategies might represent a novel therapy for AILT.

Link information
DOI
https://doi.org/10.1111/j.1365-2141.2008.07534.x
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000262826400008&DestApp=WOS_CPL
ID information
  • DOI : 10.1111/j.1365-2141.2008.07534.x
  • ISSN : 0007-1048
  • Web of Science ID : WOS:000262826400008

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