A novel marker of ameloblastoma and systematic review of immunohistochemical findings.

This study aims at investigating the pathogenesis and oncogenesis of ameloblastoma. Being the commonest odontogenic tumor with idiopathic nature, ameloblastoma poses a fierce controversy about its oncogenesis. Immunohistochemical markers, over years, have highlighted specific pathways which are inherently undertaken in the tumorigenic process of ameloblastoma. Besides the recently pronounced clue of BRAF V600E mutant gene, this study introduces a new marker with its outstanding impact on our contemporary knowledge about ameloblastoma. Extrapolating from the systematic review of medical literature and recruiting a novel immunohistochemical marker, ameloblastoma enacts a new scenario supporting the approved involvement of MAPK by overexpressing WT1 a total of 37 archival cases, regardless of the histological variant in study. There evinces a significant contribution of Wilm's tumor gene, as an oncogene rather than a suppressor gene, to the pathogenesis of the ameloblastomatous tumorigenesis. Moreover, no ameloblastomatous histological phenotype has established, given the literature underpinned, a concrete impact on the clinical behavior. Immunohistochemical research papers which investigated tumorigenesis - although they do not quantitatively measure much- had the most significant impact on the diagnostic and prognostic levels. WT1 may play, therefore, a remarkable role in the oncogenesis of ameloblastoma.

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

BACKGROUND: Ameloblastoma (AM) and odontogenic Keratocyst (OKC) are destructive odontogenic lesions of the gnathion. Although their exact pathogeneses are not yet totally understood, the viral etiopathogenesis in AM and KCOT has been proposed. True to syndromic keratocystic odontogenic tumor (sKCOT) and non-syndromic OKC is the high recurrence rate. OBJECTIVES: Given that shared pathways trailed by AM and by sKCOT/OKC have been suggested, this study, however, contrasts the expression of AM and OKC for viral antibodies. METHOD: A total of archival 80 paraffin blocks of cases of parakeratinized odontogenic keratocyst (non-syndromic KCOTs) and of ameloblastomas (n = 40 for each) were included in this study to be sectioned and stained for two immunohistochemical markers: anti-human papillomavirus and Epstein-Barr virus-encoded latent membrane protein. RESULTS: All the submitted cases of AM and parakeratinized OKC were negative for both markers: anti-HPV and anti-LMP-1. CONCLUSIONS: Although results could have been biased, given the same ethnic group and territory examined in this study, all cases were negative for both markers. Therefore, the viral contribution to the etiopathogenesis in AM and OKC could not be established in this study.