gms | German Medical Science

27th German Cancer Congress Berlin 2006

German Cancer Society (Frankfurt/M.)

22. - 26.03.2006, Berlin

Macrophage inflammatory protein (MIP)-2 contributes to liver resection-induced acceleration of hepatic metastatic tumor growth.

Meeting Abstract

  • corresponding author presenting/speaker Otto Kollmar - Klinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie, Universitätsklinikum des Saarlandes, Homburg/Saar, Deutschland
  • Michael D. Menger - Institut für Klinisch-Experimentelle Chirurgie, Universitätsklinikum des Saarlandes, Homburg/Saar
  • Claudia Scheuer - Institut für Klinisch-Experimentelle Chirurgie, Universitätsklinikum des Saarlandes, Homburg/Saar
  • Martin K. Schilling - Klinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie, Universitätsklinikum des Saarlandes, Homburg/Saar

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocOP397

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dkk2006/06dkk507.shtml

Published: March 20, 2006

© 2006 Kollmar et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Aim: To study the role of macrophage inflammatory protein (MIP)-2 in liver resection-induced acceleration of tumor growth in a mouse model of hepatic metastasis.

Methods: After a 50% hepatectomy, 1 x 105 CT26.WT cells were implanted into the left liver lobe of syngeneic BALB/c mice (PHx). Additional animals were treated with a monoclonal antibody (MAB452) neutralizing MIP-2 (PHx+mAB). Non-resected and non-mAB-treated mice (Con) served as controls. After 7 days, tumor angiogenesis and microcirculation as well as cell proliferation, tumor growth and CXCR-2 expression were analyzed using intravital fluorescence microscopy, histology, immunohistochemistry and flow cytometry.

Results: Partial hepatectomy increased (P<0.05) the expression of the MIP-2 receptor CXCR-2 on tumor cells when compared with non-resected controls, and markedly accelerated (P<0.05) angiogenesis and metastatic tumor growth. Neutralization of MIP-2 by MAB452 treatment significantly (P<0.05) depressed CXCR-2 expression. Further, the blockade of MIP-2 reduced the angiogenic response (P<0.05) and inhibited tumor growth (P<0.05). Of interest, liver resection-induced hepatocyte proliferation was not effected by anti-MIP-2 treatment.

Conclusion: Our study demonstrates that MIP-2 significantly contributes to liver resection-induced acceleration of colorectal CT26.WT hepatic metastasis growth.