TY - JOUR T1 - Analysis of p53 Protein by PAb240, Ki-67 Expression and Human Papillomavirus DNA Detection in Different Types of Odontogenic Keratocyst JF - Anticancer Research JO - Anticancer Res SP - 175 LP - 181 VL - 26 IS - 1A AU - MIGUEL A. GONZÁLEZ-MOLES AU - ADALBERTO MOSQUEDA-TAYLOR AU - MIGUEL DELGADO-RODRÍGUEZ AU - GUILLERMO MARTÍNEZ-MATA AU - JOSÉ ANTONIO GIL-MONTOYA AU - MARCO ANTONIO DÍAZ-FRANCO AU - JOSÉ JAVIER BRAVO-PÉREZ AU - NABILA M-GONZÁLEZ Y1 - 2006/01/01 UR - http://ar.iiarjournals.org/content/26/1A/175.abstract N2 - Objective: To investigate the possible association between alterations in the p53 system and human papillomavirus (HPV) infection in the etiology of odontogenic keratocysts (OKCs) and to study proliferation and epithelial maturation patterns by topographic analysis of Ki-67 expression. Materials and Methods: Eighty-three OKC samples (29 cases associated with nevoid basal cell carcinoma syndrome, 29 solitary non-recurrent cases 20 solitary recurrent cases, and 5 chondroid keratocysts) were studied by immunohistochemistry to detect p53 protein (PAb 244) and Ki-67 (MIB-1) expression, and by PCR to detect HPV DNA. Results: Twelve cases (14.6%) expressed p53 protein; no case showed the presence of HPV DNA; 9 cases (11%) presented with mild epithelial dysplasia. The suprabasal expression of Ki-67 was significantly more frequent than its basal expression (p<0.001). p53 protein expression was significantly associated with the presence of epithelial dysplasia (p=0.023). Ki-67 expression was not associated with OKC type, the presence of dysplasia, or p53 expression. Conclusion: HPVs do not participate in the etiology of OKC, and it appears unlikely that a p53 gene mutation mechanism plays a major role in the genesis of OKC. OKCs show proliferation and genuine maturation behavior reminiscent of benign neoplasms with local destructive capacity. Copyright© 2006 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved ER -