title: Over-expression of ICAM-1, VCAM-1 and ELAM-1 might influence tumor progression in colorectal cancer.
abstract: Adhesion molecules might play a role in tumor progression. We investigated expression of the adhesion molecules ICAM-1, VCAM-1 and ELAM-1 in 24 primary colorectal carcinomas using immuno-histochemistry and Northern blot analysis. Normal colonic tissue from the same patients served as controls. ICAM-1 immunostaining was restricted to the intercellular matrix and vascular endothelial cells. The vast majority of normal tissue samples revealed only faint ICAM-1 immunoreactivity. However, moderate to strong immunostaining was found in 86% of cancerous sections. The ICAM-1 immunoreaction was more intense in well-differentiated carcinomas as well as in the adenomatous parts and transition zones of cancers. Similarly, the cancers exhibited markedly enhanced VCAM-1 and ELAM-1 immunostaining in the endothelial cells of small blood vessels. The intense vascular immunostaining by ICAM-1 and VCAM-1 was associated with a strong presence of CD3-positive T lymphocytes, whereas ELAM-1 immunoreactivity did not correlate with round cell infiltration. On Northern blot analysis, ICAM-1, VCAM-1 and ELAM-1 mRNA levels were increased in 67%, 57% and 63% of carcinomas, respectively, in comparison with normal tissue samples. Densitometric analysis of Northern blots revealed an increase in ICAM-1 by 2.1-fold, an increase in VCAM-1 by 3.4-fold and an increase in ELAM-1 by 2.2-fold in cancerous tissues compared to normal controls. Over-expression of ICAM-I might prevent cell-cell disruption and, hence, tumor dissemination. Furthermore, over-expression of ICAM-1 and VCAM-1, but not ELAM-1, might favor host anti-tumor defense by trafficking of lymphocytes.
authors.affiliation: Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, Switzerland.
authors.forename: C A
authors.initials: CA
authors.lastname: Maurer
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: B
authors.initials: B
authors.lastname: Kretschmann
authors.forename: S
authors.initials: S
authors.lastname: Wildi
authors.forename: C
authors.initials: C
authors.lastname: Müller
authors.forename: H
authors.initials: H
authors.lastname: Graber
authors.forename: M
authors.initials: M
authors.lastname: Schilling
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology*; D002272:Carcinoembryonic Antigen / Q000378:metabolism; D003106:Colon / Q000378:metabolism; D015179:Colorectal Neoplasms / Q000378:metabolism / Q000473:pathology*; D019040:E-Selectin / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D002272:Carcinoembryonic Antigen; D019040:E-Selectin; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1