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Article: Analysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization

TitleAnalysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization
Authors
Issue Date2001
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
Citation
Genes Chromosomes And Cancer, 2001, v. 30 n. 3, p. 254-260 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/71940
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 1.110
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFang, Yen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorGuo, Yen_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorDeng, Men_HK
dc.contributor.authorLiang, Qen_HK
dc.contributor.authorLi, Hen_HK
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorZhou, Hen_HK
dc.contributor.authorTrent, Jen_HK
dc.date.accessioned2010-09-06T06:36:43Z-
dc.date.available2010-09-06T06:36:43Z-
dc.date.issued2001en_HK
dc.identifier.citationGenes Chromosomes And Cancer, 2001, v. 30 n. 3, p. 254-260en_HK
dc.identifier.issn1045-2257en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71940-
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.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250en_HK
dc.relation.ispartofGenes Chromosomes and Canceren_HK
dc.rightsGenes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCarcinoma, Squamous Cell - geneticsen_HK
dc.subject.meshChromosome Aberrations - geneticsen_HK
dc.subject.meshChromosome Deletionen_HK
dc.subject.meshChromosome Disordersen_HK
dc.subject.meshDNA, Neoplasm - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNasopharyngeal Neoplasms - geneticsen_HK
dc.subject.meshNucleic Acid Hybridization - methodsen_HK
dc.titleAnalysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridizationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1045-2257&volume=30&issue=3&spage=254&epage=260&date=2001&atitle=Analysis+of+genetic+alterations+in+primary+nasopharyngeal+carcinoma+by+comparative+genomic+hybridizationen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/1098-2264(2000)9999:9999<::AID-GCC1086>3.0.CO;2-Den_HK
dc.identifier.pmid11170282-
dc.identifier.scopuseid_2-s2.0-0035154261en_HK
dc.identifier.hkuros100395en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035154261&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue3en_HK
dc.identifier.spage254en_HK
dc.identifier.epage260en_HK
dc.identifier.isiWOS:000166849300005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFang, Y=7403457405en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridGuo, Y=37070141200en_HK
dc.identifier.scopusauthoridSham, JST=24472255400en_HK
dc.identifier.scopusauthoridDeng, M=55201790300en_HK
dc.identifier.scopusauthoridLiang, Q=7102360486en_HK
dc.identifier.scopusauthoridLi, H=14420042900en_HK
dc.identifier.scopusauthoridZhang, H=7409194743en_HK
dc.identifier.scopusauthoridZhou, H=38062649800en_HK
dc.identifier.scopusauthoridTrent, J=7201692482en_HK
dc.identifier.issnl1045-2257-

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