Abstract
Oral cancer is commonly preceded by premalignant lesions and conditions. The clinician's ability to identify lesions at an increased risk of cancer development is critical for its control. The purpose of this study was to compare the expression of tumor suppressor gene p53, proliferation marker Ki-67, and oncogene c-erbB2 and to evaluate the relevance of their co-expression in the diagnosis of, and prognosis for, oral leukoplakia. In the present study, the expression of biomarkers was studied immunohistochemically in 55 cases of leukoplakia (26 without dysplasia, 29 with dysplasia) and 10 cases of normal epithelia. The Labeling Indices (LI) of p53 and Ki-67 were found to increase significantly with an increase in the grade of dysplasia. A significant correlation was also found between the LI of p53 and that of Ki-67. It was also observed that c-erbB2 expression was only cytoplasmic, indicating incomplete receptor degradation. Hence, it can be concluded from the present study that the increased expression of p53 and Ki-67 with an increase in the grade of dysplasia suggests that their co-expression may be used for the identification of high-risk lesions. Also, c-erbB2 has no pathogenetic role in early carcinogenesis in the studied population, although incomplete receptor degradation, as evidenced by cytoplasmic staining, may indicate an early change.
Highlights
Oral cancer is most commonly associated with clinically definable premalignant lesions and conditions
The clinical types and sites of lesions did not correlate with the degree of dysplasia
The expression of both p53 and Ki-67 was observed as brown granular nuclear staining. The distribution of both biomarkers was limited to basal and parabasal layers in cases of leukoplakia without dysplasia, but extended to the suprabasal layers in cases with dysplasia
Summary
Oral cancer is most commonly associated with clinically definable premalignant lesions and conditions. In India, the most prevalent are leukoplakia and oral submucous fibrosis.[1] The presence of epithelial dysplasia is generally accepted as one of the most important predictors of malignant development in premalignant lesions. A better understanding of the fundamental molecular biology of the process of cancer development in the oral cavity through stages, conventionally defined as epithelial dysplasia / carcinoma in situ, may be the only way to improve our possibilities for predicting malignant development from precursor lesions.[2]. Activation of oncogenes, inactivation of tumor suppressor genes, and increased cellular proliferation are some of the key events in the multistep process of carcinogenesis. It is referred to as a tumor suppres- Located on chromosome 17p13.1 in the human genome, and encoding a 53-kDa nuclear phosphoprotein, the p53 gene has been aptly termed the “Guardian of the Genome”.3 It is referred to as a tumor suppres-
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