Expression and distribution of id helix-loop-helix proteins in human astrocytic tumors
Article first published online: 17 APR 2002
Copyright © 2002 Wiley-Liss, Inc.
Volume 38, Issue 4, pages 329–338, June 2002
How to Cite
Vandeputte, D. A.A., Troost, D., Leenstra, S., Ijlst-Keizers, H., Ramkema, M., Bosch, D. A., Baas, F., Das, N. K. and Aronica, E. (2002), Expression and distribution of id helix-loop-helix proteins in human astrocytic tumors. Glia, 38: 329–338. doi: 10.1002/glia.10076
- Issue published online: 17 APR 2002
- Article first published online: 17 APR 2002
- Manuscript Accepted: 20 FEB 2002
- Manuscript Received: 5 NOV 2001
- National Epilepsy Fund Power of the Small and Hersenstichting Nederland. Grant Number: NEF 02-10
- Stichting AZUA
- inhibitors of DNA binding;
- tumor blood vessels immunocytochemistry
The Id family of helix-loop-helix proteins is involved in a variety of processes, such as development, proliferation, and angiogenesis. In this study, we investigated the expression pattern of Id1, Id2, and Id3 in surgical specimens of human glial tumors. Western blot analysis demonstrated that all three Id proteins were expressed in astrocytic tumors. Expression levels in high-grade tumors were higher than in low-grade tumors. Immunohistochemical analysis confirmed that many of the tumor astrocytes exhibited strong Id1-3 IR. In contrast, in adult human normal brain, Id expression was low both in resting astrocytes and in endothelial cells. In tumor cells, Id proteins displayed cytoplasmic as well as nuclear localization. Id1-3 IR scores in tumor cells were positively correlated with proliferation indices. Moreover, Id1-3 IR was detected in endothelial cells of the astrocytic tumor blood vessels. The vascular Id1-3 expression correlated positively with tumor vascularity and grade. These results support the role of the Id gene family in the enhanced proliferative potential of tumor astrocytes. The evidence also supports the involvement of the Id gene family in tumor angiogenesis, a process that critically influences the malignant behavior of glial tumors. GLIA 38:329–338, 2002. © 2002 Wiley-Liss, Inc.