Immunohistochemical study of p53 and angiogenesis in benign and preneoplastic oral lesions and oral squamous cell carcinoma.

OBJECTIVES

Mutation of the p53 gene and overexpression of its protein are frequent in human cancer, suggesting that these events play a critical role in the onset or progression of many types of tumors. Angiogenesis also has been demonstrated to be associated with tumor progression, aggressiveness, and metastases. This study aimed to investigate-in normal oral epithelium, hyperplasia, dysplasia, and invasive oral squamous cell carcinoma-the prevalence of p53 protein immunoreactivity and of angiogenesis, and to determine the correlation between them.

STUDY DESIGN

The study was performed on tissue sections of hyperplasia (n = 14), dysplasia (n = 10), and invasive squamous cell carcinoma (n = 21). Seven normal samples of oral mucosa were used as control. Angiogenesis and p53 protein expression were investigated by means of immunohistochemistry.

RESULTS

This study showed that p53 protein was confined to the basal cell layer in normal oral mucosa and in the hyperplastic group. In the dysplastic group, it was expressed in the basal and suprabasal layer, whereas in invasive carcinoma, it was detected in central and peripheral regions. The percentage of p53-positive cells was evaluated, and statistically significant differences were found between normal oral mucosa and severe dysplasia, between normal mucosa and invasive carcinoma, and between mild and severe dysplasia. p53 expression showed no significant correlation with tumor grading. Angiogenesis was assessed using the endothelial cell marker von Willebrand's factor. The number and size of blood vessels increased from normal oral epithelium through dysplastic epithelium to reach a maximum in invasive carcinoma.

CONCLUSION

Angiogenesis and p53 protein immunoreactivity increased with progression from normal mucosa to invasive carcinoma, and both factors were directly correlated to each other suggesting that they may play a critical role in oral carcinogenesis.