Cyclin D1 an early biomarker in oral carcinogenesis

细胞周期蛋白D1是口腔癌发生的早期生物标志物

阅读:1

Abstract

BACKGROUND: Dysregulation of cell cycle is a fundamental hallmark of cancer progression. Cyclin D1, part of complex molecular system regulating G1-S point of cell cycle is overexpressed in variety of tumors. AIMS: To look for its immunohistochemical expression in clinically normal mucosa from patients with and without tobacco habits, leukoplakia; and correlate its expression to individual atypical morphologic features, as seen in hematoxylin and eosin (H and E) sections of leukoplakia exhibiting dysplasia. MATERIALS AND METHODS: We examined the expression of cyclin D1 in immunohistochemically stained sections of 15 normal buccal mucosa without any habits (group 1), 30 clinically normal mucosa from tobacco habituιs (group 2) and 30 leukoplakias exhibiting dysplasias (group 3). Descriptive statistical analysis performed. Results presented on Mean ± Standard deviation and in number (%). Adjusted Wald 95% Confidence Interval (CI) computed, percentages of morphological features assessed by Laplace estimate. Mann-Whitney U, Kruskal-Wallis test used to find the percentage expression of cyclin D1. RESULTS: Expression of cyclin D1 in group 3 was significantly higher than in group 1 and 2 (P < 0.001, P = 0.028), expression in group 2 was significantly higher than in group 1 (P = 0.003) and were statistically significant. Generally expression of cyclin D1 was confined to lower one-third of epithelium and was highest in mild dysplasias. Among 13 atypical morphologic features, cyclin D1 expression consistently correlated with basilar hyperplasia. CONCLUSION: The altered pattern of cyclin D1 expression here may be an early event in conversion of normal epithelium into dysplastic epithelium and may serve as a biomarker of oral carcinogenesis. Its expression may be increased in tobacco habitués. Basilar hyperplasia should be given additional weightage in the grading system in predicting the fate of affected epithelium.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。