Abstract

Oral cancer is among the top three types of cancers in India. Most invasive oral carcinomas are preceded by a pre-invasive stage, that may last for many years. . Understanding the molecular mechanisms involved in the initiation and progression to malignancy of oral cancer will help to improve its prognosis and in the elaboration of new forms of treatment. The most common genetic alterations, include gene amplication and overexpression of oncogenes such as myc, erbB-2, Epidermal Growth Factor Receptor (EGFR), Cyclin D1 and mutations, deletions and hypermethylation leading to p16 and p53 tumor suppressor gene inactivation. There still remains the problem of differentiating epitheliomatous hyperplasia from squamous cell carcinoma (SCC) especially on biopsies. AIMS: 1. To study and evaluate the expression of p53 and Cyclin D1 in oral SCC and epithelial hyperplasia. 2. To correlate the expression of p53 and Cyclin D1 in different grades of oral SCC. SETTINGS AND DESIGN:Cross-sectional study conducted over a period of 18 months. METHODS AND MATERIAL: 30 cases (n=30) of oral squamous cell carcinoma & 30 cases (n=30) of epithelial hyperplasia diagnosed on H & E were included in this study. All these cases of oral SCC were further classied into different histological grades according to BRODERS' HISTOLOGICALGRADE. STATISTICAL ANALYSIS: The data was collected and the association between different groups was analysed by using Chi square test and quantitative variables were compared using Independent Ttest/Mann-Whitney Test (when the data sets were not normally distributed) between the two groups and ANOVA/Kruskal Wallis test between three groups. Ap value of ≤0.05 was considered statistically signicant. RESULTS: There was a signicant increase in the expression of p53 in oral SCC compared to epithelial hyperplasia. The results were statistically signicant (p value <0.0001). Similarly , Cyclin D1 also showed an increased expression in cases of SCC in contrast to epithelial hyperplasia (p value <0.0001). The expression of p53 signicantly increased with increase in grade of the tumor. The results being statistically signicant, p value=0.004. Similarly, poorly and moderately differentiated SCC also showed an increased expression of Cyclin D1 compared to well differentiated SCC (p value=0.03, statistically signicant). CONCLUSION: Thus the author concludes that the expression of both p53 and Cyclin D1 is increased in oral SCC compared to epithelial hyperplasia of oral mucosa and these markers can be used to differentiate between these two lesion especially on biopsy cases.

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