Expression of CKs was consistent with other histological variants of ameloblastoma (AM), but AM-BC had significantly higher p53 and Ki-67 (p < 0.05) labeling indices than other histological variants of AM.Two patients had BRAF gene mutations.
There was no statistical difference in PCNA intensity of staining between ameloblastomas and AOTs (P > 0.05), whereas the p53 intensity in ameloblastomas was stronger than AOTs (P < 0.05).
All the other loci analyzed were altered in less than 40% of cases and some of them (D3S1312, D3S1300, IFNA, D9S164, D13S176 and TP53) did not show alterations in any of the ameloblastomas analyzed.
To clarify the role of p53 homologs in oncogenesis and cytodifferentiation of odontogenic tumors, expression of p63 and p73 was analyzed in ameloblastomas as well as tooth germs.
TP53 status was analyzed by yeast functional assay and DNA sequencing in 12 cases of ameloblastoma which were diagnosed histologically and represented the clinical features of a benign tumor.
Forty-five examples of epithelial odontogenic lesions (9 ameloblastomas (AB): 13 odontogenic keratocysts (OKC): 15 dentigerous cysts (DC): 6 radicular cysts (RC): and 2 odontogenic carcinomas (OC)) were immunohistochemically analyzed for the presence of p53 protein (p53P) and proliferative activity as indicated by positivity for Ki-67 antigen. p53P+ cells, detected as dense and/or faint nuclear staining, were found in 42 of the 45 odontogenic lesions examined.