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ORIGINAL ARTICLE
Year : 2012  |  Volume : 8  |  Issue : 2  |  Page : 232-237

Overexpression of MDM2 protein in ameloblastomas as compared to adenomatoid odontogenic tumor


1 Department of Oral and Maxillofacial Pathology, S.V.S Institute of Dental Sciences, Mahabubnagar, Andhra Pradesh, India
2 Department of Oral and Maxillofacial Pathology, S.D.M College of Dental Sciences and Hospital, Dharwad, India
3 Department of Oral and Maxillofacial Pathology, Sri Hasanamba Dental College and Hospital, Hassan, India
4 Department of Oral and Maxillofacial Pathology, Farooqia Dental College and Hospital, Mysore, Karnataka, India

Correspondence Address:
A Krishna
Department of Oral and Maxillofacial Pathology, S.V.S Institute of Dental Sciences, Appanapally, Yenugonda, Mahabubnagar, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.98976

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Background: Recent studies on odontogenic tumors have identified various molecular alterations responsible for their development, and determination of epithelial proliferation is a useful means of investigating the differences in biologic behavior of these tumors. One such specific marker to identify proliferative activity and tumor aggressiveness by immunohistochemistry (IHC) is MDM2, 90-95kDa protein. Objective: This immunohistochemical study using MDM2 expression was undertaken to understand better the diverse biological activity of two groups of odontogenic tumors namely ameloblastoma and adenomatoid odontogenic tumor (AOT) based on their cell proliferation activity. Materials and Methods: A total of 50 cases, comprising of 36 ameloblastoma samples and 14 AOT samples, were subjected to heat-induced antigen retrieval method using citrate buffer in a pressure cooker. Consequently, the sections were stained with MDM2 monoclonal antibody and visualized using an LSAB+ kit. Results: In ameloblastomas, statistically significant association was seen between plexiform ameloblastomas, follicular ameloblastomas with granular cell changes, desmoplastic and unicystic variants. The predominant nuclear staining by MDM2 revealed overexpression in ameloblastomas as compared to AOT. Conclusion: The MDM2 overexpression noticed in plexiform ameloblastoma, follicular ameloblastoma with granular cell changes and acanthomatous ameloblastoma when compared to simple unicystic and desmoplastic ameloblastoma suggest a relatively enhanced proliferative phenotype of these solid multicystic variants of ameloblastomas. On overall comparison, higher expression was noted in ameloblastomas when compared to AOT. This indicates differences in the aggressive nature between these two groups of odontogenic tumors favoring the perception of a greater aggressive nature of ameloblastomas.


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