4.5 Article

Adhesion molecules in human pancreatic cancer

Journal

JOURNAL OF SURGICAL ONCOLOGY
Volume 79, Issue 2, Pages 93-100

Publisher

WILEY
DOI: 10.1002/jso.10053

Keywords

pancreatic cancer; metastasis; adhesion molecules; ICAM-1; ELAM-1; VCAM-1

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Background and Objectives: Adhesion molecules are cell surface glycoproteins that are important in cell-to-cell and cell-to-extracellular matrix interactions. In the present study, we analyzed the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion niolecule-1), and ELAM-1 (endothelial leukocyte adhesion molecule-1) in human pancreatic cancer. Methods: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues. mRNA expression encoding ICAM-1, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry. Results: Northern blot analysis revealed a 5.4-fold increase of ICAM-1 (P < 0.0 1) and a 3.7-fold increase in VCAM-1 (P < 0.0 1) mRNA expression in cancer samples in comparison with normal controls. In contrast, ELAM-1 niRNA levels did not show significant differences between the cancer and the normal tissues. Immunohistochemical analysis of cancer tissues showed strong immunostaining for ICAM-1 and VCAM-1, and faint immunostaining for ELAM-1 in the pancreatic cancer cells. Fibrotic or noncancerous pancreatic tissue adjacent to the cancer mass was devoid of any immunoreactivity for ICAM-1, ELAM-1, and VCAM-1. In contrast, the normal pancreas exhibited no immunoreactivity of ICAM-1, ELAM-1, and VCAM-1. Conclusions: Enhanced expression of ICAM-1 and VCAM-1 in human pancreatic cancers suggests a role in tumor pathogenesis. The increase of these adhesion molecules might influence the detachment of cancer cells in the primary tumor, might contribute to cancer cell migration and the spread of cancer cells to distant organs, or both. J. Surg. Oncol. 2002;79:93-100. (C) 2002 Wiley-Liss, Inc.

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