OBJECTIVE: 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.
OBJECTIVE: 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.
Authors: Enikő Palkó; Szilárd Póliska; Zsuzsanna Csákányi; Gábor Katona; Tamás Karosi; Frigyes Helfferich; András Penyige; István Sziklai Journal: Biomed Res Int Date: 2014-02-10 Impact factor: 3.411