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Article: Analysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization
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TitleAnalysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization
 
AuthorsFang, Y3
Guan, XY2
Guo, Y
Sham, JST2
Deng, M2
Liang, Q1
Li, H3
Zhang, H2 1
Zhou, H1
Trent, J2
 
Issue Date2001
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
 
CitationGenes Chromosomes And Cancer, 2001, v. 30 n. 3, p. 254-260 [How to Cite?]
DOI: http://dx.doi.org/10.1002/1098-2264(2000)9999:9999<::AID-GCC1086>3.0.CO;2-D
 
AbstractTo identify genetic alterations associated with the development and progression of human nasopharyngeal carcinoma (NPC), 57 tumors were analyzed by comparative genomic hybridization (CGH). In 47 cases, chromosomal imbalances were found. Several recurrent chromosomal abnormalities were identified in the present study. The most frequently detected chromosomal gains involved chromosome arms 12q (24 cases, 51%), 4q (17 cases, 36%), 3q (16 cases, 34%), 1q (15 cases, 32%), and 18q (15 cases, 32%). Common regions of gain involved 12q13-q15, 4q12-q21, and 3q21-q26. High-copy-number increases of chromosomal materials were detected in four chromosomal regions, 3q21-q26.2, 4p12-q21, 8p, and 12q14-q15. The most frequently detected loss of chromosomal materials involved chromosome arms 16q (26 cases, 55%), 14q (21 cases, 45%), 1p (20 cases, 43%), 3p (20 cases, 43%), 16p (19 cases, 40%), 11q (17 cases, 36%), and 19p (16 cases, 34%). The most common regions of loss involved 14q24-qter, 1pter-p36.1, 3p22-p21.3, 11q21-qter, and the distal region of 19p. Genomic alterations detected by CGH were compared and found to be largely consistent with those identified in banding analysis and loss of heterozygosity studies. However, several previously unrecognized recurrent alterations were also identified in the present study, including gain of 4q and 18q, and loss of 16q, 14q, and 19p. In addition, gain of 1q, 8q, 18q, and loss of 9q showed a statistically significant association with advanced clinical stages (P < 0.05). Identification of recurrent sites of chromosomal gain and loss identify regions of the genome that may contain oncogenes or tumor suppressor genes, respectively, which may be involved in the tumorigenesis of NPC.
 
ISSN1045-2257
2012 Impact Factor: 3.546
2012 SCImago Journal Rankings: 1.774
 
DOIhttp://dx.doi.org/10.1002/1098-2264(2000)9999:9999<::AID-GCC1086>3.0.CO;2-D
 
ISI Accession Number IDWOS:000166849300005
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorFang, Y
 
dc.contributor.authorGuan, XY
 
dc.contributor.authorGuo, Y
 
dc.contributor.authorSham, JST
 
dc.contributor.authorDeng, M
 
dc.contributor.authorLiang, Q
 
dc.contributor.authorLi, H
 
dc.contributor.authorZhang, H
 
dc.contributor.authorZhou, H
 
dc.contributor.authorTrent, J
 
dc.date.accessioned2010-09-06T06:36:43Z
 
dc.date.available2010-09-06T06:36:43Z
 
dc.date.issued2001
 
dc.description.abstractTo identify genetic alterations associated with the development and progression of human nasopharyngeal carcinoma (NPC), 57 tumors were analyzed by comparative genomic hybridization (CGH). In 47 cases, chromosomal imbalances were found. Several recurrent chromosomal abnormalities were identified in the present study. The most frequently detected chromosomal gains involved chromosome arms 12q (24 cases, 51%), 4q (17 cases, 36%), 3q (16 cases, 34%), 1q (15 cases, 32%), and 18q (15 cases, 32%). Common regions of gain involved 12q13-q15, 4q12-q21, and 3q21-q26. High-copy-number increases of chromosomal materials were detected in four chromosomal regions, 3q21-q26.2, 4p12-q21, 8p, and 12q14-q15. The most frequently detected loss of chromosomal materials involved chromosome arms 16q (26 cases, 55%), 14q (21 cases, 45%), 1p (20 cases, 43%), 3p (20 cases, 43%), 16p (19 cases, 40%), 11q (17 cases, 36%), and 19p (16 cases, 34%). The most common regions of loss involved 14q24-qter, 1pter-p36.1, 3p22-p21.3, 11q21-qter, and the distal region of 19p. Genomic alterations detected by CGH were compared and found to be largely consistent with those identified in banding analysis and loss of heterozygosity studies. However, several previously unrecognized recurrent alterations were also identified in the present study, including gain of 4q and 18q, and loss of 16q, 14q, and 19p. In addition, gain of 1q, 8q, 18q, and loss of 9q showed a statistically significant association with advanced clinical stages (P < 0.05). Identification of recurrent sites of chromosomal gain and loss identify regions of the genome that may contain oncogenes or tumor suppressor genes, respectively, which may be involved in the tumorigenesis of NPC.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationGenes Chromosomes And Cancer, 2001, v. 30 n. 3, p. 254-260 [How to Cite?]
DOI: http://dx.doi.org/10.1002/1098-2264(2000)9999:9999<::AID-GCC1086>3.0.CO;2-D
 
dc.identifier.doihttp://dx.doi.org/10.1002/1098-2264(2000)9999:9999<::AID-GCC1086>3.0.CO;2-D
 
dc.identifier.epage260
 
dc.identifier.hkuros100395
 
dc.identifier.isiWOS:000166849300005
 
dc.identifier.issn1045-2257
2012 Impact Factor: 3.546
2012 SCImago Journal Rankings: 1.774
 
dc.identifier.issue3
 
dc.identifier.openurl
 
dc.identifier.pmid11170282
 
dc.identifier.scopuseid_2-s2.0-0035154261
 
dc.identifier.spage254
 
dc.identifier.urihttp://hdl.handle.net/10722/71940
 
dc.identifier.volume30
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
 
dc.publisher.placeUnited States
 
dc.relation.ispartofGenes Chromosomes and Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsGenes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshAdult
 
dc.subject.meshAged
 
dc.subject.meshCarcinoma, Squamous Cell - genetics
 
dc.subject.meshChromosome Aberrations - genetics
 
dc.subject.meshChromosome Deletion
 
dc.subject.meshChromosome Disorders
 
dc.subject.meshDNA, Neoplasm - analysis
 
dc.subject.meshFemale
 
dc.subject.meshHumans
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshNasopharyngeal Neoplasms - genetics
 
dc.subject.meshNucleic Acid Hybridization - methods
 
dc.titleAnalysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization
 
dc.typeArticle
 
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<description.abstract>To identify genetic alterations associated with the development and progression of human nasopharyngeal carcinoma (NPC), 57 tumors were analyzed by comparative genomic hybridization (CGH). In 47 cases, chromosomal imbalances were found. Several recurrent chromosomal abnormalities were identified in the present study. The most frequently detected chromosomal gains involved chromosome arms 12q (24 cases, 51%), 4q (17 cases, 36%), 3q (16 cases, 34%), 1q (15 cases, 32%), and 18q (15 cases, 32%). Common regions of gain involved 12q13-q15, 4q12-q21, and 3q21-q26. High-copy-number increases of chromosomal materials were detected in four chromosomal regions, 3q21-q26.2, 4p12-q21, 8p, and 12q14-q15. The most frequently detected loss of chromosomal materials involved chromosome arms 16q (26 cases, 55%), 14q (21 cases, 45%), 1p (20 cases, 43%), 3p (20 cases, 43%), 16p (19 cases, 40%), 11q (17 cases, 36%), and 19p (16 cases, 34%). The most common regions of loss involved 14q24-qter, 1pter-p36.1, 3p22-p21.3, 11q21-qter, and the distal region of 19p. Genomic alterations detected by CGH were compared and found to be largely consistent with those identified in banding analysis and loss of heterozygosity studies. However, several previously unrecognized recurrent alterations were also identified in the present study, including gain of 4q and 18q, and loss of 16q, 14q, and 19p. In addition, gain of 1q, 8q, 18q, and loss of 9q showed a statistically significant association with advanced clinical stages (P &lt; 0.05). Identification of recurrent sites of chromosomal gain and loss identify regions of the genome that may contain oncogenes or tumor suppressor genes, respectively, which may be involved in the tumorigenesis of NPC.</description.abstract>
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Author Affiliations
  1. National Human Genome Research Institute
  2. The University of Hong Kong
  3. Sun Yat Sen University of Medical Sciences