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Kahlert, C.* ; Weber, H.* ; Mogler, C.* ; Bergmann, F.* ; Schirmacher, P.* ; Kenngott, H.G.* ; Matterne, U.* ; Mollberg, N.* ; Rahbari, N.N.* ; Hinz, U.* ; Koch, M.* ; Aigner, M.* ; Weitz, J.*

Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse.

Br. J. Cancer 101, 457-464 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
BACKGROUND: ALCAM (activated leucocyte cell adhesion molecule, synonym CD166) is a cell adhesion molecule, which belongs to the Ig superfamily. Disruption of the ALCAM-mediated adhesiveness by proteolytic sheddases such as ADAM17 has been suggested to have a relevant impact on tumour invasion. Although the expression of ALCAM is a valuable prognostic and predictive marker in several types of epithelial tumours, its role as a prognostic marker in pancreatic cancer has not yet been reported. METHODS: In this study, paraffin-embedded samples of 97 patients with pancreatic cancer undergoing potentially curative resection were immunostained against ALCAM, ADAM17 and CK19. Expression of ALCAM and ADAM17 was semiquantitatively evaluated and correlated to clinical and histopathological parameters. RESULTS: We could show that in normal pancreatic tissue, ALCAM is predominantly expressed at the cellular membrane, whereas in pancreatic tumour cells, it is mainly localised in the cytoplasm. In addition, univariate and multivariate analyses show that increased expression of ALCAM is an adverse prognostic factor for recurrence-free and overall survival. Overexpression of ADAM17 in pancreatic cancer, however, failed to be a significant prognostic marker and was not coexpressed with ALCAM. CONCLUSIONS: Our findings support the hypothesis that the disruption of ALCAM-mediated adhesiveness is a relevant step in pancreatic cancer progression. Moreover, ALCAM overexpression is a relevant independent prognostic marker for poor survival and early tumour relapse in pancreatic cancer.
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Publication type Article: Journal article
Document type Scientific Article
Language english
Publication Year 2009
HGF-reported in Year 0
ISSN (print) / ISBN 0007-0920
e-ISSN 1532-1827
Quellenangaben Volume: 101, Issue: 3, Pages: 457-464 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Reviewing status Peer reviewed
Institute(s) Institute of Pancreatic Islet Research (IPI)
PubMed ID 19603023
Erfassungsdatum 2009-12-31