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Title: Abundant copy-number loss of CYCLOPS and STOP genes in gastric adenocarcinoma
Authors: Cutcutache I. 
Wu A.Y.
Suzuki Y. 
McPherson J.R. 
Lei Z. 
Deng N. 
Zhang S. 
Wong W.K. 
Soo K.C. 
Chan W.H. 
Ooi L.L. 
Welsch R.
Tan P. 
Rozen S.G. 
Keywords: DNA
allelic imbalance
cancer inhibition
controlled study
copy number alterations yielding cancer liabilities owing to partial loss gene
copy number variation
down regulation
gene expression regulation
gene targeting
genetic association
heterozygosity loss
human cell
human tissue
microarray analysis
priority journal
single nucleotide polymorphism
stomach adenocarcinoma
stomach carcinogenesis
suppressor of tumorigenesis or proliferation gene
tumor suppressor gene
cell proliferation
gene dosage
gene expression regulation
stomach tumor
Cell Proliferation
Gene Dosage
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
Loss of Heterozygosity
Polymorphism, Single Nucleotide
Stomach Neoplasms
Issue Date: 2016
Publisher: Springer Tokyo
Citation: Cutcutache I., Wu A.Y., Suzuki Y., McPherson J.R., Lei Z., Deng N., Zhang S., Wong W.K., Soo K.C., Chan W.H., Ooi L.L., Welsch R., Tan P., Rozen S.G. (2016). Abundant copy-number loss of CYCLOPS and STOP genes in gastric adenocarcinoma. Gastric Cancer 19 (2) : 453-465. ScholarBank@NUS Repository.
Abstract: Background: Gastric cancer, a leading cause of cancer death worldwide, has been little studied compared with other cancers that impose similar health burdens. Our goal is to assess genomic copy-number loss and the possible functional consequences and therapeutic implications thereof across a large series of gastric adenocarcinomas. Methods: We used high-density single-nucleotide polymorphism microarrays to determine patterns of copy-number loss and allelic imbalance in 74 gastric adenocarcinomas. We investigated whether suppressor of tumorigenesis and/or proliferation (STOP) genes are associated with genomic copy-number loss. We also analyzed the extent to which copy-number loss affects Copy-number alterations Yielding Cancer Liabilities Owing to Partial losS (CYCLOPS) genes–genes that may be attractive targets for therapeutic inhibition when partially deleted. Results: The proportion of the genome subject to copy-number loss varies considerably from tumor to tumor, with a median of 5.5 %, and a mean of 12 % (range 0–58.5 %). On average, 91 STOP genes were subject to copy-number loss per tumor (median 35, range 0–452), and STOP genes tended to have lower copy-number compared with the rest of the genes. Furthermore, on average, 1.6 CYCLOPS genes per tumor were both subject to copy-number loss and downregulated, and 51.4 % of the tumors had at least one such gene. Conclusions: The enrichment of STOP genes in regions of copy-number loss indicates that their deletion may contribute to gastric carcinogenesis. Furthermore, the presence of several deleted and downregulated CYCLOPS genes in some tumors suggests potential therapeutic targets in these tumors. © 2015, The Author(s).
Source Title: Gastric Cancer
ISSN: 14363291
DOI: 10.1007/s10120-015-0514-z
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