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article · Egyptian Dental Journal /Egyptian Dental Journal

Double Immunohistochemical Analysis of PCNA and FAK Expression in Selected Odontogenic Lesions

Abstract

Background: Odontogenic neoplasms and cysts have diverse biological behaviors, ranging from indolence to aggressive spectrum. The proliferating cell nuclear antigen (PCNA) is involved in DNA synthesis and proliferation. Focal adhesion kinase (FAK) is associated with cellular signaling, growth, and invasion. PCNA and FAK have been shown to be involved in neoplastic proliferation, invasion, and migration. Thereby, double immunohistochemical assay of PCNA and FAK could be a predictive tool evaluating the level of aggressiveness of odontogenic lesions. Methods: The current study was conducted to evaluate the expressions of PCNA and FAK. A double immunohistochemistry for ameloblastoma (AB), unicystic AB, calcifying epithelial odontogenic tumor (CEOT), and glandular odontogenic cyst (GOC) was used to evaluate both markers and assess their role in the aggressiveness of selected lesions. All formalin-fixed paraffin-embedded blocks (n = 10) for each group were double PCNA and FAK immunostained and then assessed using a transmission light microscope and an image-analyzer computer system. Statistical analysis was performed with a one-way analysis of variance test followed by Tukey’s post hoc test. Results: All study groups showed nuclear immunoreactivity of PCNA and cytoplasmic immunoreactivity for FAK. The greatest mean nuclear count of PCNA and the greatest mean area percent for FAK were both recorded in the aggressive lesions; i.e., the CEOT and AB groups. Conclusions: In conclusion, PCNA and FAK immunoexpression profiles may have a strong correlation with the aggressive nature of AB, CEOT, and GOC. Hence, PCNA and FAK markers could aid in their routine examination, treatment planning, and prognosis.

Research topics

  • Oral and Maxillofacial Pathology
  • Head and Neck Surgical Oncology
  • Salivary Gland Tumors Diagnosis and Treatment

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DOI: 10.21608/edj.2023.190709.2421

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