INTRODUCTION: Odontogenic tumors are a variety of oral lesions with clinical and histological variability. Some are benign, while others, like ameloblastoma, show infiltrative behavior. The most aggressive destructive odontogenic tumor is ameloblastic carcinoma. Diagnostic challenges arise in differentiating a malignant type from a classic benign ameloblastoma due to overlapping clinicopathologic features, prompting the use of immunohistochemical methods. KIAA0101, a nucleoprotein, is crucial for cell proliferation regulation, and its expression as a prognostic marker is being extensively researched in various human tumor sorts. However, its role in odontogenic tumors still needs more diagnostic research to be approved. Aim of the study: Evaluation of KIAA0101 immunoexpression in ameloblastoma and ameloblastic carcinoma. MATERIAL AND METHODS: Sixty blocks of human odontogenic tissues, divided equally into enamel organs (serving as a normal control), ameloblastoma, and ameloblastic carcinoma, were included in the study. Sections were stained with hematoxylin and eosin to determine an accurate histopathological diagnosis. Immunohistochemical analysis using the KIAA0101 antibody was performed using universal immunostaining techniques. RESULTS: Different immunoexpression of KIAA0101 were expressed in enamel organs, ameloblastoma, and ameloblastic carcinoma. The enamel organs showed the lowest expression levels, while the highest were detected in ameloblastic carcinoma. CONCLUSION: KIAA0101 produced a valuable indicator for tissue proliferation in ameloblastoma and ameloblastic carcinoma.
Research Abstract	
              Research Date	
              Research Department	
              
          Research File	
          
      Research Journal	
              Alexandria Dental Journal
          Research Member	
          
      Research Publisher	
              Alexandria University; Faculty of Dentistry
          Research Vol	
              50
          Research Website	
              https://adjalexu.journals.ekb.eg/article_365695.html
          Research Year	
              2024
          Research Pages	
              1-7
           
          