Abstract
Background: The tumor suppressor protein p16 plays a vital role in the regulation of the cell cycle. The expression of p16 was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. Materials and Methods: Tissue sections ranging from normal oral mucosa to moderately differentiated oral squamous cell carcinoma (OSCC) were studied immunohistochemically. Results: In normal rats p16 expression increased gradually during oral oncogenesis, but a significant increase was observed only in moderately differentiated OSCC (p=0.038). On the contrary, in diabetic rats the detected gradual increase was significant in hyperplasia, dysplasia, early invasion and well-differentiated OSCC (p<0.001). Nevertheless, there was no significant difference in p16 expression during oral oncogenesis between normal and diabetic animals. Conclusion: It seems that the expression of cell cycle regulator p16 is not affected by diabetes in the studied animal model of oral oncogenesis.
Footnotes
- Received April 23, 2007.
- Revision received June 14, 2007.
- Accepted June 22, 2007.
- Copyright © 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved