Authors J. West and T. A. Munoz-Antonia have contributed equally to the preparation of this manuscript.
Transforming Growth Factor-β Type II Receptors and Smad Proteins in Follicular Thyroid Tumors †
Article first published online: 2 JAN 2009
Copyright © 2000 The Triological Society
Volume 110, Issue 8, pages 1323–1327, August 2000
How to Cite
West, J., Munoz-Antonia, T., G. Johnson, J., Klotch, D. and Muro-Cacho, C. A. (2000), Transforming Growth Factor-β Type II Receptors and Smad Proteins in Follicular Thyroid Tumors . The Laryngoscope, 110: 1323–1327. doi: 10.1097/00005537-200008000-00019
- Issue published online: 2 JAN 2009
- Article first published online: 2 JAN 2009
- Manuscript Accepted: 9 FEB 2000
- Transforming growth factor-β;
- Smad proteins;
- follicular thyroid tumors.
Objective Resistance to transforming growth factor (TGF)-β–mediated cell growth inhibition is a well-known pathogenic mechanism in epithelial neoplasia. TGF-β signaling requires normal function of downstream mediators such as TGF-β receptors (TβRs) and Smad proteins. The goal of this study is to investigate the expression of components of the TGF-β signaling pathway in follicular tumors of the thyroid.
Study Design Twenty follicular thyroid neoplasms were classified as adenomas (11) or minimally invasive follicular carcinomas (9) according to current pathological criteria. Protein expression was evaluated to identify differences between benign and malignant tumors that could be used as an adjunct to histopathological analysis.
Methods Paraffin-embedded tissue sections containing tumor and adjacent nonneoplastic parenchyma were analyzed by immunohistochemistry for the expression of TβR type II (TβR-II) and Smad2, Smad4, Smad6, and Smad7. Expression of each protein in the tumor was compared with that of the corresponding adjacent nonneoplastic thyroid parenchyma.
Results TβR-II expression was lost in 78% of the carcinomas. In the remaining 22%, TβR-II was preserved but Smad2 expression was lost. In all conventional adenomas, however, TβR-II expression was maintained. Furthermore, all tumors with normal expression of all proteins were adenomas.
Conclusions Downregulation of TβR-II is a consistent abnormality in follicular carcinomas and can be used to differentiate minimally invasive carcinomas from adenomas. Also, downregulation of Smad proteins is another mechanism by which carcinomas can become independent from TGF-β–mediated growth inhibition.