Vairaktaris Eleftherios, Goutzanis Lambros, Nkenke Emeka, Spyridonidou Sofia, Vassiliou Stavros, Derka Spyridoula, Vylliotis Antonis, Yapijakis Christos, Lazaris Andreas, Patsouris Efstratios
Department of Oral and Maxillofacial Surgery, University of Athens Medical School, Athens 11521, Greece.
In Vivo. 2007 Sep-Oct;21(5):745-50.
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.
Tissue sections ranging from normal oral mucosa to moderately differentiated oral squamous cell carcinoma (OSCC) were studied immunohistochemically.
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.
It seems that the expression of cell cycle regulator p16 is not affected by diabetes in the studied animal model of oral oncogenesis.
肿瘤抑制蛋白p16在细胞周期调控中起着至关重要的作用。在正常和糖尿病（I型）斯普拉格-道利大鼠化学诱导致癌的实验模型中，对p16的表达进行了研究。
采用免疫组织化学方法研究了从正常口腔黏膜到中度分化口腔鳞状细胞癌（OSCC）的组织切片。
在正常大鼠中，p16表达在口腔肿瘤发生过程中逐渐增加，但仅在中度分化的OSCC中观察到显著增加（p = 0.038）。相反，在糖尿病大鼠中，在增生、发育异常、早期浸润和高分化OSCC中检测到的逐渐增加具有显著性（p < 0.001）。然而，正常和糖尿病动物在口腔肿瘤发生过程中p16表达没有显著差异。
在研究的口腔肿瘤发生动物模型中，细胞周期调节因子p16的表达似乎不受糖尿病的影响。
