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Title: Consistent and differential genetic aberrations between esophageal dysplasia and squamous cell carcinoma detected by array comparative genomic hybridization
Authors: Shi, Z.-Z
Shang, L
Jiang, Y.-Y 
Hao, J.-J
Zhang, Y
Zhang, T.-T
Lin, D.-C 
Liu, S.-G
Wang, B.-S
Gong, T
Zhan, Q.-M
Wang, M.-R
Keywords: cyclin dependent kinase inhibitor 2A
advanced cancer
ANO1 gene
cancer staging
CCND1 gene
cdkn2a gene
cell proliferation
cell strain
cell strain KYSE30
cell strain KYSE510
chromosome 11q
chromosome 7p
comparative genomic hybridization
controlled study
esophageal squamous cell carcinoma
esophagus biopsy
esophagus dysplasia
esophagus resection
gene amplification
gene deletion
gene dosage
gene identification
gene loss
gene overexpression
genetic disorder
human cell
human tissue
lymph node metastasis
major clinical study
microarray analysis
priority journal
protein expression
real time polymerase chain reaction
RNA analysis
Carcinoma, Squamous Cell
Cell Line, Tumor
Chromosome Aberrations
Comparative Genomic Hybridization
DNA Copy Number Variations
Esophageal Neoplasms
Gene Amplification
Gene Deletion
Gene Expression
Precancerous Conditions
Issue Date: 2013
Citation: Shi, Z.-Z, Shang, L, Jiang, Y.-Y, Hao, J.-J, Zhang, Y, Zhang, T.-T, Lin, D.-C, Liu, S.-G, Wang, B.-S, Gong, T, Zhan, Q.-M, Wang, M.-R (2013). Consistent and differential genetic aberrations between esophageal dysplasia and squamous cell carcinoma detected by array comparative genomic hybridization. Clinical Cancer Research 19 (21) : 5867-5878. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Purpose: Our aim was to identify frequent genomic aberrations in both esophageal squamous cell carcinoma (ESCC) and esophageal dysplasia and to discover important copy number-driving genes and microRNAs (miRNA) in ESCC. Experimental Design: We conducted array-based comparative genomic hybridization (array CGH) on 59 ESCCresection samples and 16 dysplasia biopsy samples. Expression of genes at 11q13.3 was analyzed by real-time PCR (RT-PCR) and immunohistochemistry (IHC). Integrated analysis was conducted to identify genes or miRNAs with copy number-expression correlations. Results: Array CGH identified 11 amplifications and eight homozygous deletions in ESCC. Integrated analysis of array CGH data with matched gene expression microarray data showed that 90 overexpressed genes and 24 underexpressed genes were consistent with DNA copy number changes, including 12 copy number-driving miRNAs. In esophageal dysplasia, six gains, four losses, 12 amplifications, and four homozygous deletions were detected. Amplifications of 7p11.2 and 11q13.2-11q13.3 (CCND1) and homozygous deletion at 9p21.3 (CDKN2A) were consistent genomic changes in both dysplasia and carcinoma. ANO1 at 11q13.3 was overexpressed at the mRNA and protein levels in tumors, and higher mRNA expression was correlated with the copy number increase. In particular, ANO1 expression was elevated in moderate dysplasia compared with normal esophageal epithelium. IHC revealed that ANO1 overexpression was positively correlated with lymph node metastasis and advanced clinical stage. Knockdown of ANO1 significantly inhibited the proliferation of KYSE30 and KYSE510 cells. Conclusion: Copy number aberrations in both esophageal dysplasia and ESCC may be useful as potential biomarkers for early detection. In addition, ANO1 may be a candidate target gene in esophageal tumorigenesis. © 2013 American Association for Cancer Research.
Source Title: Clinical Cancer Research
ISSN: 1078-0432
DOI: 10.1158/1078-0432.CCR-12-3753
Rights: Attribution 4.0 International
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