Cyclin D1 an early biomarker in oral carcinogenesis

J Oral Maxillofac Pathol. 2013 Sep;17(3):351-7. doi: 10.4103/0973-029X.125189.

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.

Keywords: Cell cycle; cyclin D1; epithelial dysplasia; oral carcinogenesis; tobacco.