help button home button Am J Pathol ASIP WHAT IS IT?
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Renkonen, R.
Right arrow Articles by Gahmberg, C. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Renkonen, R.
Right arrow Articles by Gahmberg, C. G.

American Journal of Pathology, Vol 140, 763-767, Copyright © 1992 by American Society for Investigative Pathology


REGULAR ARTICLES

Expression of endothelial adhesion molecules in vivo. Increased endothelial ICAM-2 expression in lymphoid malignancies

R Renkonen, T Paavonen, P Nortamo and CG Gahmberg
Department of Bacteriology, University of Helsinki, Finland.

The authors have compared the reactivity of monoclonal antibodies (MAb) directed against endothelial adhesion molecules (ICAM-1, ICAM-2, VCAM- 1, ELAM-1) in hyperplastic, nonmalignant, and malignant lymph nodes. The authors demonstrate that the reactivity with ICAM-1 MAb is stronger in the high endothelial venules (HEV) and other smaller vessels (SV) in lymphomas compared with hyperplastic lymph nodes. Similarly, the reactivity of an ICAM-2 MAb (6D5) was shown to be higher in malignant lymph nodes compared with nonmalignant ones. ICAM-2 MAb stained both the HEV and SV. VCAM-1 MAb reacted strongly with germinal centers and its endothelial reactivity was higher in the lymphoma nodes. ELAM-1 MAb stained only faintly some endothelial cells in malignant tissue. These data suggest that besides the known regulatable endothelial adhesion molecules ICAM-1 and VCAM-1, the expression of ICAM-2 can be modified.


This article has been cited by other articles:


Home page
JNCI J Natl Cancer InstHome page
A. Dienst, A. Grunow, M. Unruh, B. Rabausch, J. E. Nor, J. W. U. Fries, and C. Gottstein
Specific Occlusion of Murine and Human Tumor Vasculature by VCAM-1-Targeted Recombinant Fusion Proteins
J Natl Cancer Inst, May 18, 2005; 97(10): 733 - 747.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
A. W. Griffioen, M. J.H. Coenen, C. A. Damen, S. M.M. Hellwig, D. H.J. van Weering, W. Vooys, G. H. Blijham, and G. Groenewegen
CD44 Is Involved in Tumor Angiogenesis; an Activation Antigen on Human Endothelial Cells
Blood, August 1, 1997; 90(3): 1150 - 1159.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
L. Heiska, C. Kantor, T. Parr, D. R. Critchley, P. Vilja, C. G. Gahmberg, and O. Carpen
Binding of the Cytoplasmic Domain of Intercellular Adhesion Molecule-2 (ICAM-2) to alpha -Actinin
J. Biol. Chem., October 18, 1996; 271(42): 26214 - 26219.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
K. Somersalo, O. Carpén, E. Saksela, C. G. Gahmberg, P. Nortamo, and T. Timonen
Activation of Natural Killer Cell Migration by Leukocyte Integrin-binding Peptide from Intracellular Adhesion Molecule-2 (ICAM-2)
J. Biol. Chem., April 14, 1995; 270(15): 8629 - 8636.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1992 by the American Society for Investigative Pathology.