Abstract

The sample comprised of 20 odontogenic keratocysts (OKC), 20 ameloblastomas (AM), and 15 adenomatoid odontogenic tumors (AOT) specimens. Nuclear and cytoplasmic immunolabeling of ING3 and ING4 were semi-quantitatively evaluated in epithelial cells of the odontogenic lesions, according to the percentage of immunolabelled cells in each case. Descriptive and statistics analysis were computed, and the p-value was set at 0.05. No statistically significant differences were found in cytoplasmic and nuclear ING3 immunolabeling among the studied lesions. In contrast, AOTs presented higher cytoplasmic and nuclear ING4 labeling compared to AMs (cytoplasmic p-value = 0.01; nuclear p-value < 0.001) and OKCs (nuclear p-value = 0.007). ING3 and ING4 protein downregulation may play an important role in the initiation and progression of more aggressive odontogenic lesions, such as AMs and OKCs.

Highlights

  • A large variety of lesions arises in the maxillary bones

  • Considering the involvement of tumor suppressor genes in the development of tumors, in order to better understand the role of these markers in the development and biological behavior of odontogenic lesions, the present study aimed to evaluate the immunohistochemical profiles of ING3 and ING4 proteins in a series of benign epithelial odontogenic lesions

  • A wide range of epithelium associated factors have been implicated in the biological behavior of these lesions, including increased expression of various proliferative markers, impaired expression of tumor suppressor genes and their products, and abnormal cell cycle pathways

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Summary

Introduction

A large variety of lesions arises in the maxillary bones. Among them, cysts and odontogenic tumors, which originate from epithelial cell remnants of the dental germ [1]. Odontogenic keratocysts (OKCs) and ameloblastomas (AMs) are frequently associated with their aggressive behaviors and high recurrence potential [2]. For this reason, despite the fact that OKC presents a cystic nature, many studies are currently underway to clarify the molecular mechanisms involved in the peculiar behavior of this lesion [3]. The biological behavior of any lesion is highly dependent on its proliferative activity, and on cell death rates. Proteins from the tumor suppressor gene family, called Inhibitors of Growth (ING), have been associated with cell cycle control, cell senescence, replication, DNA repair, cell proliferation, apoptosis and angiogenesis. In contrast to ING1 and ING2, which functionality is already well stablished, conflicting data have been reported concerning ING3 and ING4 role in neoplasms [8]

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