Evidence from intra-patient progression indicates adenoid ameloblastoma as a phenotypic variant of dentinogenic ghost cell tumor.

Adenoid ameloblastoma (AA) and dentinogenic ghost cell tumor (DGCT) show marked morphologic and molecular overlap but remain classified as distinct odontogenic entities largely on the basis of architectural predominance. We studied 3 patients with ghost cell odontogenic lesions who underwent sequential resections, permitting longitudinal intra-patient analysis of progression from calcifying odontogenic cyst (COC) or DGCT to ghost cell odontogenic carcinoma (GCOC). Adenomatoid differentiation and ghost cell/dentinoid components were quantitatively assessed across stages. Immunohistochemistry for β-catenin, BRAF V600E, and Ki-67 and Sanger sequencing of CTNNB1 exon 3 were performed. All cases showed marked architectural plasticity, with dynamic shifts in adenomatoid and ghost cell/dentinoid proportions during recurrence and malignant transformation. By contrast, molecular findings remained stable within each patient. Nuclear β-catenin accumulation persisted at all stages, BRAF V600E was uniformly negative, and proliferative activity increased with transformation to GCOC. These findings provide longitudinal evidence that architectural predominance in ghost cell odontogenic lesions is dynamic rather than fixed and support the interpretation that AA may represent an adenomatoid-predominant phenotype within the DGCT spectrum.