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Clinical and Translational Oncology
Published in: Clinical and Translational Oncology 7/2014

01-07-2014 | Research Article

Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma

Authors: Z.-Z. Shi, Y.-Y. Jiang, J.-J. Hao, Y. Zhang, T.-T. Zhang, L. Shang, S.-G. Liu, F. Shi, M.-R. Wang

Published in: Clinical and Translational Oncology | Issue 7/2014

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Abstract

Background

Genomic aberration is a common feature of human cancers and also is one of the basic mechanisms that lead to overexpression of oncogenes and underexpression of tumor suppressor genes. Our study aims to identify frequent genomic changes and candidate copy number driving genes in esophageal squamous cell carcinoma (ESCC).

Methods

We used array comparative genomic hybridization to identify recurrent genomic alterations and screened the candidate targets of selected amplification regions by quantitative and semi-quantitative RT-PCR.

Results

Thirty-four gains and 16 losses occurred in more than 50 % of ESCCs. High-level amplifications at 7p11.2, 8p12, 8q24.21, 11q13.2-q13.3, 12p11.21, 12q12 and homozygous deletions at 2q22.1, 8p23.1-p21.2, 9p21.3 and 14q11.2 were also identified. 11q13.2 was a frequent amplification region, in which five genes including CHKA, GAL, KIAA1394, LRP5 and PTPRCAP were overexpressed in tumor tissues than paracancerous normal tissues. The expression of ALG3 at 3q27.1 was higher in ESCCs, especially in patients with lymph node metastasis.

Conclusions

Target gene identification of amplifications or homozygous deletions will help to reveal the mechanism of tumor formation and explore new therapy method.
Appendix
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Metadata
Title
Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma
Authors
Z.-Z. Shi
Y.-Y. Jiang
J.-J. Hao
Y. Zhang
T.-T. Zhang
L. Shang
S.-G. Liu
F. Shi
M.-R. Wang
Publication date
01-07-2014
Publisher
Springer Milan
Published in
Clinical and Translational Oncology / Issue 7/2014
Print ISSN: 1699-048X
Electronic ISSN: 1699-3055
DOI
https://doi.org/10.1007/s12094-013-1124-z

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