Abstract
Oral leukoplakia (OL) is a white lesion of an indeterminate risk not related to any excluded (other) known diseases or disorders that carry no increased risk for cancer. Many biological markers have been used in an attempt to predict malignant transformation; however, no reliable markers have been established so far. Objective To evaluate cell proliferation and immortalization in OL, comparing non-dysplastic (Non-dys OL) and dysplastic OL (Dys OL).Methodology This is a cross-sectional observational study. Paraffin-embedded tissue blocks of 28 specimens of Non-dys OL, 33 of Dys OL, 9 of normal oral mucosa (NOM), 17 of inflammatory hyperplasia (IH), and 19 of oral squamous cell carcinomas (OSCC) were stained for Ki-67 and BMI-1 using immunohistochemistry.Results A gradual increase in BMI-1 and K-i67 expression was found in oral carcinogenesis. The immunolabeling for those markers was higher in OSCC when compared with the other groups (Kruskal-Wallis, p<0.05). Ki-67 expression percentage was higher in OL and in IH when compared with NOM (Kruskal-Wallis/Dunn, p<0.05). Increased expression of BMI-1 was also observed in OL when compared with NOM (Kruskal-Wallis/Dunn, p<0.05). No differences were observed in expression of both markers when non-dysplastic and dysplastic leukoplakias were compared. A significant positive correlation between Ki-67 and BMI-1 was found (Spearman correlation coefficient, R=0.26, p=0.01). High-grade epithelial dysplasia was associated with malignant transformation (Chi-squared, p=0.03).Conclusions These findings indicate that BMI-1 expression increases in early oral carcinogenesis and is possibly associated with the occurrence of dysplastic changes. Furthermore, our findings indicate that both Ki-67 and BMI-1 are directly correlated and play a role in initiation and progression of OSCC.
Highlights
Oral leukoplakia (OL) is a lesion with a risk of malignant transformation ranging from 0.13% to 17.5%.1 Histopathologically, OL is characterized by a variety of epithelial changes, including dysplasia
Our findings indicate that both Ki-67 and BMI-1 are directly correlated and play a role in initiation and progression of oral squamous cell carcinomas (OSCC)
Many biological markers have been explored, no reliable ones have yet been established for predicting malignant transformation of OL, necessitating additional studies to increase our knowledge of the biological processes underlying OL and oral carcinogenesis
Summary
Oral leukoplakia (OL) is a lesion with a risk of malignant transformation ranging from 0.13% to 17.5%.1 Histopathologically, OL is characterized by a variety of epithelial changes, including dysplasia. Many biological markers have been explored, no reliable ones have yet been established for predicting malignant transformation of OL, necessitating additional studies to increase our knowledge of the biological processes underlying OL and oral carcinogenesis.. Ki-67 expression correlates with the severity of epithelial dysplasia and histological grading of oral squamous cell carcinoma (OSCC).. Ki-67 expression correlates with the severity of epithelial dysplasia and histological grading of oral squamous cell carcinoma (OSCC).6,7 Another protein named BMI-1, which mediates gene silencing by regulating chromatin structure, plays a central role in cell cycle regulation and cell immortalization, as well as cell senescence and epithelial-mesenchymal transition (EMT).. Increased BMI-1 expression was found in bronchial premalignant lesions as well as squamous cell carcinoma (SCC), indicating that its expression in neoplastic cells may be an early event in lung carcinogenesis.. Increased BMI-1 expression was found in bronchial premalignant lesions as well as squamous cell carcinoma (SCC), indicating that its expression in neoplastic cells may be an early event in lung carcinogenesis. BMI-1 is overexpressed in OSCC cells when compared with normal oral mucosa cells and has been presumed to influence proliferation and immortalization of epithelial cells in oral carcinogenesis.
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