Öztürk, KayhanYıldırım, Mahmut SelmanAcar, HasanCenik, ZiyaKeleş, Bahar2020-03-262020-03-262006Öztürk, K., Yıldırım, M. S., Acar, H., Cenik, Z., Keleş, B., (2006). Evaluation of c-MYC Status in Primary Acquired Cholesteatoma by Using Fluorescence in Situ Hybridization Technique. Otology & Neurotology, (27), 588-591. Doi: 10.1097/01.mao.0000226290.04048.d91531-7129https://dx.doi.org/10.1097/01.mao.0000226290.04048.d9https://hdl.handle.net/20.500.12395/20480Objective: The object of study was to investigate the status of c-MYC oncogene in primary acquired cholesteatoma. Study design: Descriptive study. Methods: Cholesteatoma samples were obtained from 15 patients with primary acquired cholesteatoma during surgical operation. Fluorescence in situ hybridization with a mixed DNA probe, which is specific for c-MYC located on 8q24 and chromosome 8 specific-alpha-satellite DNA probe (dual color), was used on the interphase nuclei. Results: Copy number of c-MYC oncogene and aneuploidy of chromosome 8 were 21.2% +/- 14.4% and 21.7% +/- 14.8%, respectively. There was no significant difference between copy number of c-MYC and frequency of chromosome 8 aneuploidy (p > 0.05). Ten of 15 cases showed different percentage of c-MYC and chromosome 8 aneuploidy, whereas 5 (33.3%) of 15 cases showed a normal distribution of c-MYC and chromosome 8 signals. Conclusion: The copy number of c-MYC in 10 of 15 cases was found to be high as observed for chromosome 8 aneuploidy in primary acquired cholesteatoma. These findings suggest that the ability of hyperproliferation of primary acquired cholesteatoma might have been related to c-MYC copy number by deregulating c-MYC expression.en10.1097/01.mao.0000226290.04048.d9info:eu-repo/semantics/openAccessaneuploidycholesteatomachromosome 8c-MYCFISHoncogeneArticle2758859116868505Q1WOS:000239528500003Q2