Affiliations: Department of Pathology, University of Campinas/UNICAMP, Campinas, Brazil | Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands | Department of Pathology, IUOPA, Hospital Universitario Central de Asturias, Oviedo, Spain | Department of Otolaryngology, IUOPA, Hospital Universitario Central de Asturias, Oviedo, Spain
Note: [] Corresponding author: Ana Flávia Costa, Departamento de Anatomia Patológica, Faculdade de Ciências Médicas, UNICAMP, Rua Tessália Vieira de Camargo 126, 13084-971 Campinas, São Paulo, Brazil. Tel.: +55 19 32893897; E-mail: costa.anaflavia@ gmail.com.
Abstract: Background: ACC can occasionally undergo dedifferentiation also referred to as high-grade transformation (ACC-HGT). However, ACC-HGT can also undergo transformation to adenocarcinomas which are not poorly differentiated. ACC-HGT is generally considered to be an aggressive variant of ACC, even more than solid ACC. This study was aimed to describe the genetic changes of ACC-HGT in relation to clinico-pathological features and to compare results to solid ACC. Methods: Genome-wide DNA copy number changes were analyzed by microarray CGH in ACC-HGT, 4 with transformation into moderately differentiated adenocarcinoma (MDA) and two into poorly differentiated carcinoma (PDC), 5 solid ACC. In addition, Ki-67 index and p53 immunopositivity was assessed. Results: ACC-HGT carried fewer copy number changes compared to solid ACC. Two ACC-HGT cases harboured a breakpoint at 6q23, near the cMYB oncogene. The complexity of the genomic profile concurred with the clinical course of the patient. Among the ACC-HGT, p53 positivity significantly increased from the conventional to the transformed (both MDA and PDC) component. Conclusion: ACC-HGT may not necessarily reflect a more advanced stage of tumor progression, but rather a transformation to another histological form in which the poorly differentiated forms (PDC) presents a genetic complexity similar to the solid ACC.
