Expression of Ki-67, p53 and p63 proteins in keratocyst odontogenic tumours: an immunohistochemical study

Aim To investigate the immunohistochemical expression of Ki-67, p53 and p63 in Keratocyst Odontogenic Tumours (KOTs) in order to contribute to the biological profile of this tumor. Methods Immunohistochemical technique was performed using the EnVision™ System in 37 cases of KOTs. Results Ki-67- and...

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Bibliographic Details
Published in:Journal of molecular histology 2008-06, Vol.39 (3), p.311-316
Main Authors: Gurgel, Clarissa Araújo Silva, Ramos, Eduardo Antônio Gonçalves, Azevedo, Roberto Almeida, Sarmento, Viviane Almeida, da Silva Carvalho, Ana Maria, dos Santos, Jean Nunes
Format: Article
Language:English
Subjects:
Antibodies
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cell Count
Developmental Biology
Humans
Immunohistochemistry
Ki-67 Antigen - metabolism
Life Sciences
Odontogenic Cysts - metabolism
Odontogenic Cysts - pathology
Odontogenic Tumors - metabolism
Odontogenic Tumors - pathology
Original Paper
Trans-Activators - metabolism
Transcription Factors
Tumor Suppressor Protein p53 - metabolism
Tumor Suppressor Proteins - metabolism
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Summary:Aim To investigate the immunohistochemical expression of Ki-67, p53 and p63 in Keratocyst Odontogenic Tumours (KOTs) in order to contribute to the biological profile of this tumor. Methods Immunohistochemical technique was performed using the EnVision™ System in 37 cases of KOTs. Results Ki-67- and p53-immunostained cells were mainly located in the suprabasal layers. p63-positive cells were found throughout the lining cystic epithelium. No difference in the immunostaining for these proteins was observed between primary and recurrent KOTs (Ki-67: P  = 0.5591; p53: P  = 0.9847; p63: P  = 0.9127), or between KOTs associated with Nevoid Basal Cell Carcinoma Syndrome (NBCCS) and sporadic KOTs (Ki-67: P  = 0.7013; p53: P  = 0.3197; p63: P  = 0.2427). Conclusions It is possible that biological behavior of KOTs may be related to suprabasal proliferative compartment in the cystic epithelium as observed by high levels of Ki-67, p53 and p63. In addition, p63 immunostaining may represent immaturity of keratinocytes in KOTs, and suggests that this protein may participate in the regulation of epithelial cell differentiation. Taken together, these data may favor tumorigenesis on KOTs.
ISSN:1567-2379
1567-2387
DOI:10.1007/s10735-008-9167-0