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Central giant cell lesion of the jaws: study of CCND1 gene amplification and p16INK4a protein levels |
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| Authors: | Renato Luiz Maia Nogueira Mário Henrique Girão Faria Rafael Lima Verde Osterne Roberta Barroso Cavalcante Ronaldo Albuquerque Ribeiro Cassiano Francisco Weege Nonaka Silvia Helena Barem Rabenhorst |
| Affiliation: | 1. Department of Dental Clinic, Discipline of Oral and Maxillofacial Surgery and Stomatology, Federal University of Ceara School of Dentistry, Fortaleza, Brazil 2. Department of Oral and Maxillofacial Surgery, Memorial Batista Hospital, Fortaleza, Brazil 3. Department of Pathology and Forensic Medicine, Molecular Genetics Laboratory (LABGEM), School of Medicine, Federal University of Ceará, Fortaleza, Brazil 4. Department of Pathology, Fortaleza University School of Medicine, Av. Washington Soares, 1321, Edson Queiroz, P.O. Box 1258, Fortaleza, Ceará, 60811-905, Brazil 5. Department of Oral and Maxillofacial Pathology, Fortaleza University School of Dentistry, Fortaleza, Brazil 6. Department of Physiology and Pharmacology, Federal University of Ceara School of Medicine, Fortaleza, Brazil 7. Department of Dentistry, Center for Biological and Health Sciences, State University of Paraiba, Paraíba, Brazil 8. Department of Pathology and Forensic Medicine, Molecular Genetics Laboratory (LABGEM), School of Medicine, Federal University of Ceara, Fortaleza, Brazil |
| Abstract: | Central giant cell lesions (CGCLs) are uncommon benign jaw lesions with uncertain etiology and a variable clinical behavior. In neoplasms, alterations in molecules involved in the G1/S checkpoint are frequently found. Loss of p16INK4a expression or overexpression of cyclin D1 may stimulate cell proliferation. The purpose of this study was to analyze CCND1 gene amplification and the expression of p16INK4a in CGCLs. Structural analysis of the CCND1 was performed using chromogenic in situ hybridization. Immmunohistochemistry was used to identify p16INK4a protein levels. Statistical analysis correlated the two biomarkers with clinical behavior and between each other. Twenty-four lesions were included, being 11 aggressive and 13 non-aggressive. Moderate/high-level CCND1 amplification was found in 12 lesions. Also, immunoreactivity for p16INK4a was present in 12 cases, mainly in mononuclear cells. There was a significantly higher level of p16INK4a expression in mononuclear cells of non-aggressive lesions and lesions with moderate/high-level CCND1 amplification in mononuclear cells. It could be speculated that some CGCLs may develop as a true benign neoplasm. The higher expression of p16INK4a in non-aggressive lesions and in cases with moderate/high-level CCND1 amplification may show that these molecules have a role in CGCLs. |
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