Hypermethylation of p16 Tumor-Suppressor Gene in Ameloblastic Carcinoma, Ameloblastoma, and Dental Follicles

Ameloblastic carcinoma: a Brazilian collaborative study of 17 cases

“…Ki67 expression and p53 expression have been found to be increased in AMECA as compared with AME . Our study showed that p16 is highly expressed in AMECA, in apparent disagreement with the presence of CpG methylation of p16 found in AMECA in the study of Khojasteh et al . Thus, more studies are needed to improve our understanding of these molecular events.…”

“…Other authors have also suggested that high expression of α‐smooth muscle actin and decreased expression of syndecan‐1 in AMECA may serve as an indicator of tumour aggressiveness and high metastatic potential . We believe that the immunohistochemical panel described above should be further evaluated in order to identify its relevance in diagnosing AMECA …”

“…63,67 Other authors have also suggested that high expression of a-smooth muscle actin and decreased expression of syndecan-1 in AMECA may serve as an indicator of tumour aggressiveness and high metastatic potential. [63][64][65][66][67][68] We believe that the immunohistochemical panel described above should be further evaluated in order to identify its relevance in diagnosing AMECA. [62][63][64][65][66][67][68] Because of its aggressive course, AMECA is usually treated with wide local resection with clear margins.…”

The anecdote of viral etiopathogenia in ameloblastoma and odontogenic keratocyst: Why don’t we let it go?

“…This holds true especially when it comes to naming human papilloma and Epstein-Barr viruses. [9][10][11][12][13] Therefore, this study uses a pair of immunohistochemical markers, which are expected to scrutinize the applicability of this hypothesis in AM and OKC. Moreover, this paper shall tackle re-reallocating non-syndromic KCOTs back to odontogenic keratocyst (OKC) given the WHO's controversial promotion of all OKC to KCOT in 2005.…”

Pathogenesis and Nomenclature of Odontogenic Carcinomas: Revisited

“…Therefore, it is presumed that p16 alteration may play a role in the malignant progression of ameloblastic carcinoma [40]. More recently, 5q13 amplification was demonstrated by comparative genomic hybridization (CGH) in an AC [41].…”