EGFR is not amplified in ameloblastoma

• Main Authors: Abreu Alves, F. (Author), Costa, V. (Author), Fonseca, F.P (Author), Fregnani, E.R (Author), Kaminagakura, E. (Author), Pinto, C.A.L (Author)
• Format: Article
• Language: English
• Published: Mosby Inc. 2018
• Subjects: adolescent; Adolescent; adult; Adult; aged; Aged; ameloblastoma; Ameloblastoma; Biomarkers, Tumor; child; Child; epidermal growth factor receptor; female; Female; fluorescence in situ hybridization; gene amplification; Gene Amplification; human; Humans; immunohistochemistry; Immunohistochemistry; In Situ Hybridization, Fluorescence; Ki 67 antigen; Ki-67 Antigen; male; Male; mandible tumor; Mandibular Neoplasms; metabolism; middle aged; Middle Aged; Receptor, Epidermal Growth Factor; Retrospective Studies; retrospective study; tumor marker
• Online Access: View Fulltext in Publisher

 Objective: The aim of this study was to investigate alterations in the EGFR gene and its protein expression for a better understanding of the biologic behavior of ameloblastoma. Study Design: Twenty-five samples of ameloblastoma were selected, and dual-color fluorescence in situ hybridization assay was performed. The results of the assay and immunohistochemistry reaction for EGFR and Ki67 were associated with clinicopathologic features and recurrence. Results: All analyzed cases presented disomy without any gene polysomy or amplification. With regard to EGFR immunoexpression, 3 cases (12%) were considered negative, and 22 (88%) were positive, of which 13 (52%) were weak and 9 (36%) were strong. All samples presented low positivity for Ki67. There was no association between EGFR expression and clinicopathologic features or recurrence (P >.05). In some cases, EGFR immunoexpression was observed without gene amplification. Conclusions: Ameloblastoma development, progression, or recurrence does not appear to be related to EGFR amplification or polysomy. © 2018 Elsevier Inc.