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Title in Portuguese: Central giant cell lesion of the jaws : study of CCND1 gene amplification and p16INK4a protein levels
Author: Nogueira, Renato Luiz Maia
Faria, Mário Henrique Girão
Osterne, Rafael Lima Verde
Cavalcante, Roberta Barroso
Ribeiro, Ronaldo Albuquerque
Nonaka, Cassiano Francisco Weege
Rabenhorst, Silvia Helena Barem
Keywords: Células Gigantes
Ciclina D1
Issue Date: Oct-2013
Publisher: Medicina Oral, Patología Oral y Cirugía Bucal
Citation: NOGUEIRA, R. L. M. et al. Central giant cell lesion of the jaws : study of CCND1 gene amplification and p16INK4a protein levels. Journal of Molecular Histology, v. 44, n. 5, p. 527-534, out. 2013.
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/highlevel 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/highlevel CCND1 amplification may show that these molecules have a role in CGCLs.
metadata.dc.type: Artigo de Periódico
ISSN: 1567-2379 (Print)
1567-2387 (Online)
Appears in Collections:DCOD - Artigos publicados em revistas científicas

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