gms | German Medical Science

27. Deutscher Krebskongress

Deutsche Krebsgesellschaft e. V.

22. - 26.03.2006, Berlin

Lymphatic vessel density in pancreatic carcinoma

Meeting Abstract

  • corresponding author presenting/speaker Gerald Assmann - Pathologisches Institut der Universität München, Deutschland
  • Axel KLEESPIES - Chirurgische Klinik und Poliklinik der Universität München
  • Andreas Nolte - Klinik und Poliklinik für Strahlentherapie der Universität München
  • Ralf Wilkowski - Klinik und Poliklinik für Strahlentherapie der Universität München
  • Christiane Bruns - Chirurgische Klinik und Poliklinik der Universität München
  • Joachim Diebold - Pathologisches Institut der Universität München

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocPE224

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dkk2006/06dkk334.shtml

Veröffentlicht: 20. März 2006

© 2006 Assmann et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Aims: Pancreatic carcinoma is frequently associated with lymphangiosis carcinomatosa and lymph node metastasis; however, so far it has not been studied whether pancreatic carcinomas are able to induce the formation of new lymphatic vessels. We therefore assessed the number of lymphatic vessels at the tumor margin and compared it with non-neoplastic pancreas and areas of fibrosis in the same specimens.

Methods: So far 33 patients with curatively resected carcinomas of the head of pancreas were studied by immunohistochemistry for Podoplanin, a specific marker for lymphatic endothelial cells. We counted the number of lymphatic vessels at tumor margin, in areas with fibrosis without tumor and in the preexisting pancreas (magnification 400x, per 10 HPF). For statistical analyses Shapiro-Wilks-Test and Wilcoxon-Test were performed.

Results: The median numbers of lymphatic vessels were: 3 lymphatic vessels (LV) per 10 HPF in the preexisting pancreas, 20 LV/10 HPF in fibrosis without tumor and 21.3 LV/10 HPF at the tumor margin. The differences in LV density between both fibrosis and tumor margin versus preexisting pancreas were highly significant (p<0.001), whereas the data for fibrosis and tumor margin were almost identical (p=0.985).

Conclusions: Lymphatic vessel density is increased in pancreatic carcinomas. This phenomenon seems to be part of the general peritumoral inflammatory reaction and not a result of a specific tumor-cell effect. Further investigations are in progress which (1) correlate the results with the expression of VEGF-C and VEGF-D in pancreatic carcinomas and (2) compare the observations with the lymphatic vessel density in granulation tissue and chronic pancreatitis.