Immunohistochemical detection of p53 and PCNA in ameloblastoma and adenomatoid odontogenic tumor

Abstract

Although ameloblastoma and adenomatoid odontogenic tumor (AOT) belong to the same group according to the World Health Organization, they show different biologic behaviors. PCNA, an amplifier of cell proliferation, and p53, a tumor suppressor protein, are overexpressed in some odontogenic lesions. The purpose of this study was to immunohistochemically evaluate the expression of p53 and PCNA to clarify the possible role of these proteins in different behaviors of ameloblastoma and AOT. The immunohistochemical expression of PCNA and p53 was determined in 30 solid ameloblastomas and 12 AOTs. Statistical tests including one-way ANOVA, t-test, chi-square, Mann-Whitney U and Kendall were used to analyze the data. All tissue sections (except one specimen of plexiform ameloblastoma) exhibited immunoexpression for p53. PCNA was expressed in all specimens. There was no significant difference in PCNA expression between ameloblastomas and AOTs (P > 0.05). For p53, there was no statistical difference between subtypes of ameloblastomas (P > 0.05), whereas statistical differences were observed between ameloblastomas and AOTs (P < 0.001). There was no statistical difference in PCNA intensity of staining between ameloblastomas and AOTs (P > 0.05), whereas the p53 intensity in ameloblastomas was stronger than AOTs (P < 0.05). Positive correlation between PCNA and p53 was observed. We concluded that PCNA overexpression is not responsible for the difference in clinical behavior of these two lesions, whereas the expression of p53 in ameloblastoma may explain the more aggressive nature of this tumor compared with AOT.

Current Concepts and Occurrence of Epithelial Odontogenic Tumors: I. Ameloblastoma and Adenomatoid Odontogenic Tumor

“…AOT demonstrates a similar level of PCNA immunoreaction to ameloblastomas but exhibits weaker expressions of p53 and MDM2. This implies that AOT has less aggressive behavior than ameloblastomas 86,87. In AOTs, some epithelial tumor cells show a strong cytoplasmic reaction to β-catenin,88 possess whirling epithelial cells expressing cyclin D1, and have spindle-shaped tumor cells that are positive for podoplanin 89.…”

Molecular etiopathogenesis of ameloblastoma – current concepts revisited

“…Funaoka et al found higher PCNA labeling index for follicular AB than that of plexiform ameloblastoma. Ueno et al, (1989) and Reichart et al, (1995) also stated that the high expression of PCNA in follicular AB can explain its increased potential of recurrence, but Salehinejad et al, (2011) found the highest mean Index of positivity for PCNA in acanthomatous AB. [14] The possibility of malignant transformation in recurrent cases of AB can be determined by PCNA values.…”

“…Ueno et al, (1989) and Reichart et al, (1995) also stated that the high expression of PCNA in follicular AB can explain its increased potential of recurrence, but Salehinejad et al, (2011) found the highest mean Index of positivity for PCNA in acanthomatous AB. [14] The possibility of malignant transformation in recurrent cases of AB can be determined by PCNA values. There was an increase in the expression from UA to follicular AB to plexiform AB and with maximum positivity seen in ameloblastic carcinoma, which may be correlated with biological behavior of the tumor.…”

Regulation of p53 under hypoxic and inflammatory conditions in periodontium

“…Inflammatory processes are known to increase the risk of cancer development supporting the fact that p53 is a possible Bconnecting pointb etween hypoxia, inflammation, and carcinogenesis [11]. Genetic alterations of p53 have been found in oral squamous cell carcinoma and odontogenic tumors as well as in some osteoblastomas and osteosarcomas, indicating a role in oral tumorigenesis [12,13]. Other authors have shown that p53 is an important factor in oral malodorous-induced apoptosis in periodontal tissues [14].…”