rss
J Clin Pathol 2004;57:630-636 doi:10.1136/jcp.2003.014498
  • Original article

Inflammatory cells contribute to the generation of an angiogenic phenotype in pancreatic ductal adenocarcinoma

  1. I Esposito1,
  2. M Menicagli2,
  3. N Funel2,
  4. F Bergmann1,
  5. U Boggi3,
  6. F Mosca3,
  7. G Bevilacqua2,
  8. D Campani2
  1. 1Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany
  2. 2Department of Oncology, Transplantation and Advanced Technologies in Medicine, Division of Surgical, Molecular and Ultrastructural Pathology, University of Pisa, Pisa 56100, Italy
  3. 3Department of Oncology, Transplantation and Advanced Technologies in Medicine, Division of General and Transplantation Surgery, University of Pisa
  1. Correspondence to:
 Dr I Esposito
 Institute of Pathology, University of Heidelberg, Im Neuenheimer Feld 220, 69120 Heidelberg, Germany; irene_espositomed.uni-heidelberg.de
  • Accepted 22 December 2003

Abstract

Background: Inflammatory cells contribute to the growth and spread of human malignancies by producing molecules that enhance tumour invasiveness.

Aims: To characterise the inflammatory infiltrate in pancreatic ductal adenocarcinoma and to analyse its contribution to angiogenesis and its prognostic relevance.

Methods: Immunohistochemistry was used to identify inflammatory cells and evaluate the expression of proangiogenic and prolymphangiogenic molecules (vascular endothelial growth factor A (VEGF-A), VEGF-C, and basic fibroblast growth factor (bFGF)) by inflammatory and cancer cells in 137 pancreatic cancers. Intratumorous microvessel density (IMD) was assessed using CD34 as an endothelial cell marker.

Results: There were significantly more mast cells and macrophages in pancreatic cancers than in normal pancreas and the number of mast cells directly correlated with the presence of lymph node metastases. However, there was no relation between numbers of infiltrating inflammatory cells and the presence of chronic pancreatitis (CP)-like changes in the parenchyma surrounding the tumour. Double immunostaining revealed that both pancreatic mast cells and macrophages express VEGF-A, VEGF-C, and bFGF. These factors were also expressed in the tumour cells in many cases. The numbers of VEGF-A expressing tumour cells and bFGF expressing tumour and inflammatory cells significantly correlated with IMD. Moreover, tumours with higher IMD had higher numbers of infiltrating mast cells and macrophages.

Conclusions: Mononuclear inflammatory cells of the non-specific immune response are recruited to pancreatic cancer tissues independent of the presence of CP-like changes, may influence the metastatic capacity of the cancer cells, and may contribute to the development of tumours with high angiogenic activity.

Footnotes

    This Article

    1. Abstract
    2. Full text
    3. PDF

    Responses

    1. Submit a response
    2. No responses published

    Register for free content

    The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

    Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.