Detection of C-MYC oncogene translocation and copy number change in the normal-dysplasia-carcinoma sequence of the larynx by fluorescence in situ hybridization

被引:8
|
作者
Liu, Yu [1 ,2 ]
Gong, Li-Ping [2 ]
Dong, Xiao-Li [2 ]
Liu, Hong-Gang [1 ]
机构
[1] Capital Med Univ, Dept Pathol, Beijing Tongren Hosp, Beijing 100730, Peoples R China
[2] Capital Med Univ, Dept Pathol, Beijing 100069, Peoples R China
基金
中国国家自然科学基金;
关键词
fluorescent in situ hybridization; laryngeal carcinoma; dysplasia; C-MYC; copy number change; SQUAMOUS-CELL CARCINOMA; COMPARATIVE GENOMIC HYBRIDIZATION; TISSUE MICROARRAY ANALYSIS; PARAFFIN-EMBEDDED TISSUE; CHROMOSOMAL-ABNORMALITIES; GENE AMPLIFICATION; TUMOR PROGRESSION; MOLECULAR-BIOLOGY; HEAD; NECK;
D O I
10.1002/dc.22879
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
The aim of this study was to determine the translocation and copy number change of the C-MYC gene in patients with laryngeal dysplasia and laryngeal squamous cell carcinoma (LSCC), and to evaluate the prevalence of such expression in relation to the normal-dysplasia-carcinoma sequence. Fluorescent in situ hybridization (FISH) was applied on formalin-fixed paraffin-embedded blocks of 93 laryngeal lesion specimens (14 normal epithelium, 15 mild dysplasia, 18 moderate dysplasia, 16 severe dysplasia, 9 carcinoma in situ, and 21 invasive carcinoma). C-MYC translocation was not observed in all laryngeal tissue. The high frequency for C-MYC copy-number increased (100%) in invasive carcinoma: 57.14% amplifications and 42.86% gains, and the positive rate of C-MYC amplification and copy-number change increased with the increasing severity of laryngeal lesions (P < 0.0001). The results suggest that C-MYC may be activated by gain/amplification in LSCC and precancerous lesions. Thus, C-MYC may play an important role in promoting LSCC progression, and early FISH detection of C-MYC may be exploited to set a screening test for laryngeal dysplasia. Diagn.Cytopathol. 2013. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:515 / 519
页数:5
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