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Article: Integration of DNA copy number alterations and transcriptional expression analysis in human gastric cancer
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TitleIntegration of DNA copy number alterations and transcriptional expression analysis in human gastric cancer
 
AuthorsFan, B1 4
Dachrut, S1 2
Coral, H1
Yuen, ST3
Chu, KM3
Law, S3
Zhang, L4
Ji, J4
Leung, SY3
Chen, X1
 
KeywordsComplementary DNA
Bacterial artificial chromosome
Cancer cell
Chromosome deletion
Comparative genomic hybridization
 
Issue Date2012
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2012, v. 7 n. 4 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0029824
 
AbstractBackground: Genomic instability with frequent DNA copy number alterations is one of the key hallmarks of carcinogenesis. The chromosomal regions with frequent DNA copy number gain and loss in human gastric cancer are still poorly defined. It remains unknown how the DNA copy number variations contributes to the changes of gene expression profiles, especially on the global level. Principal Findings: We analyzed DNA copy number alterations in 64 human gastric cancer samples and 8 gastric cancer cell lines using bacterial artificial chromosome (BAC) arrays based comparative genomic hybridization (aCGH). Statistical analysis was applied to correlate previously published gene expression data obtained from cDNA microarrays with corresponding DNA copy number variation data to identify candidate oncogenes and tumor suppressor genes. We found that gastric cancer samples showed recurrent DNA copy number variations, including gains at 5p, 8q, 20p, 20q, and losses at 4q, 9p, 18q, 21q. The most frequent regions of amplification were 20q12 (7/72), 20q12-20q13.1 (12/72), 20q13.1-20q13.2 (11/72) and 20q13.2-20q13.3 (6/72). The most frequent deleted region was 9p21 (8/72). Correlating gene expression array data with aCGH identified 321 candidate oncogenes, which were overexpressed and showed frequent DNA copy number gains; and 12 candidate tumor suppressor genes which were down-regulated and showed frequent DNA copy number losses in human gastric cancers. Three networks of significantly expressed genes in gastric cancer samples were identified by ingenuity pathway analysis. Conclusions: This study provides insight into DNA copy number variations and their contribution to altered gene expression profiles during human gastric cancer development. It provides novel candidate driver oncogenes or tumor suppressor genes for human gastric cancer, useful pathway maps for the future understanding of the molecular pathogenesis of this malignancy, and the construction of new therapeutic targets. © 2012 Fan et al.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0029824
 
PubMed Central IDPMC3335165
 
ISI Accession Number IDWOS:000305341000002
Funding AgencyGrant Number
University of California Cancer Research Coordinate Committee
China Scholarship Council2010601079
Funding Information:

This work is supported by the funding provided by University of California Cancer Research Coordinate Committee to XC. BF is supported by China Scholarship Council Contract No.2010601079. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorFan, B
 
dc.contributor.authorDachrut, S
 
dc.contributor.authorCoral, H
 
dc.contributor.authorYuen, ST
 
dc.contributor.authorChu, KM
 
dc.contributor.authorLaw, S
 
dc.contributor.authorZhang, L
 
dc.contributor.authorJi, J
 
dc.contributor.authorLeung, SY
 
dc.contributor.authorChen, X
 
dc.date.accessioned2012-05-29T06:14:44Z
 
dc.date.available2012-05-29T06:14:44Z
 
dc.date.issued2012
 
dc.description.abstractBackground: Genomic instability with frequent DNA copy number alterations is one of the key hallmarks of carcinogenesis. The chromosomal regions with frequent DNA copy number gain and loss in human gastric cancer are still poorly defined. It remains unknown how the DNA copy number variations contributes to the changes of gene expression profiles, especially on the global level. Principal Findings: We analyzed DNA copy number alterations in 64 human gastric cancer samples and 8 gastric cancer cell lines using bacterial artificial chromosome (BAC) arrays based comparative genomic hybridization (aCGH). Statistical analysis was applied to correlate previously published gene expression data obtained from cDNA microarrays with corresponding DNA copy number variation data to identify candidate oncogenes and tumor suppressor genes. We found that gastric cancer samples showed recurrent DNA copy number variations, including gains at 5p, 8q, 20p, 20q, and losses at 4q, 9p, 18q, 21q. The most frequent regions of amplification were 20q12 (7/72), 20q12-20q13.1 (12/72), 20q13.1-20q13.2 (11/72) and 20q13.2-20q13.3 (6/72). The most frequent deleted region was 9p21 (8/72). Correlating gene expression array data with aCGH identified 321 candidate oncogenes, which were overexpressed and showed frequent DNA copy number gains; and 12 candidate tumor suppressor genes which were down-regulated and showed frequent DNA copy number losses in human gastric cancers. Three networks of significantly expressed genes in gastric cancer samples were identified by ingenuity pathway analysis. Conclusions: This study provides insight into DNA copy number variations and their contribution to altered gene expression profiles during human gastric cancer development. It provides novel candidate driver oncogenes or tumor suppressor genes for human gastric cancer, useful pathway maps for the future understanding of the molecular pathogenesis of this malignancy, and the construction of new therapeutic targets. © 2012 Fan et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2012, v. 7 n. 4 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0029824
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0029824
 
dc.identifier.hkuros205611
 
dc.identifier.isiWOS:000305341000002
Funding AgencyGrant Number
University of California Cancer Research Coordinate Committee
China Scholarship Council2010601079
Funding Information:

This work is supported by the funding provided by University of California Cancer Research Coordinate Committee to XC. BF is supported by China Scholarship Council Contract No.2010601079. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue4
 
dc.identifier.pmcidPMC3335165
 
dc.identifier.pmid22539939
 
dc.identifier.scopuseid_2-s2.0-84859967040
 
dc.identifier.urihttp://hdl.handle.net/10722/148694
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subjectComplementary DNA
 
dc.subjectBacterial artificial chromosome
 
dc.subjectCancer cell
 
dc.subjectChromosome deletion
 
dc.subjectComparative genomic hybridization
 
dc.titleIntegration of DNA copy number alterations and transcriptional expression analysis in human gastric cancer
 
dc.typeArticle
 
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<contributor.author>Chu, KM</contributor.author>
<contributor.author>Law, S</contributor.author>
<contributor.author>Zhang, L</contributor.author>
<contributor.author>Ji, J</contributor.author>
<contributor.author>Leung, SY</contributor.author>
<contributor.author>Chen, X</contributor.author>
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Author Affiliations
  1. University of California, San Francisco
  2. Khon Kaen University
  3. The University of Hong Kong
  4. Peking University