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.
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