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Article: Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative hybridization

TitleRecurrent chromosome alterations in hepatocellular carcinoma detected by comparative hybridization
Authors
Issue Date2000
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, 2000, v. 29 n. 2, p. 110-116 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and has a very poor prognosis. Fifty primary HCC cases have been analyzed in the present study to explore the association between genomic alteration in primary HCC and clinical features. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected chromosomal gains involved chromosome arms 1q (33/50 cases, 66%), 8q (24/50 cases, 48%), and 20q (10/50 cases, 20%). High-copy-number amplifications involving lq (4 cases), 8q (3 cases), and 20q (3 cases) were detected, and a minimum overlapping amplified region at 1q12-q22 was identified. The most frequently detected loss of chromosomal material involved 16q (35/50 cases, 70%), 17p (26/50 cases, 52%), 19p (21/50 cases, 42%), 4q (20/50 cases, 40%), 1p (18/50 cases, 36%), 8p (16/50 cases, 32%), and 22q (14/50 cases, 28%). The associations between genomic alterations detected in the present study and clinical features including clinical stage, tumor size, HBV infection, chronic Fiver disease, and liver cirrhosis were explored. Our CGH results suggest that the gain of 20q and deletion of 8p are late genetic alterations in HCC, because the incidence of these alterations was obviously increased in the advanced clinical stages. Another finding showed that loss of 8p and gain of 8q and 20q are associated with tumor size. The recurrent gain and loss of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in HCC development and progression. (C) 2000 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/150754
ISSN
2014 Impact Factor: 4.041
2014 SCImago Journal Rankings: 2.106
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGuan, XYen_US
dc.contributor.authorFang, Yen_US
dc.contributor.authorSham, JSTen_US
dc.contributor.authorKwong, DLWen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLiang, Qen_US
dc.contributor.authorLi, Hen_US
dc.contributor.authorZhou, Hen_US
dc.contributor.authorTrent, JMen_US
dc.date.accessioned2012-06-26T06:09:55Z-
dc.date.available2012-06-26T06:09:55Z-
dc.date.issued2000en_US
dc.identifier.citationGenes Chromosomes And Cancer, 2000, v. 29 n. 2, p. 110-116en_US
dc.identifier.issn1045-2257en_US
dc.identifier.urihttp://hdl.handle.net/10722/150754-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and has a very poor prognosis. Fifty primary HCC cases have been analyzed in the present study to explore the association between genomic alteration in primary HCC and clinical features. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected chromosomal gains involved chromosome arms 1q (33/50 cases, 66%), 8q (24/50 cases, 48%), and 20q (10/50 cases, 20%). High-copy-number amplifications involving lq (4 cases), 8q (3 cases), and 20q (3 cases) were detected, and a minimum overlapping amplified region at 1q12-q22 was identified. The most frequently detected loss of chromosomal material involved 16q (35/50 cases, 70%), 17p (26/50 cases, 52%), 19p (21/50 cases, 42%), 4q (20/50 cases, 40%), 1p (18/50 cases, 36%), 8p (16/50 cases, 32%), and 22q (14/50 cases, 28%). The associations between genomic alterations detected in the present study and clinical features including clinical stage, tumor size, HBV infection, chronic Fiver disease, and liver cirrhosis were explored. Our CGH results suggest that the gain of 20q and deletion of 8p are late genetic alterations in HCC, because the incidence of these alterations was obviously increased in the advanced clinical stages. Another finding showed that loss of 8p and gain of 8q and 20q are associated with tumor size. The recurrent gain and loss of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in HCC development and progression. (C) 2000 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250en_US
dc.relation.ispartofGenes Chromosomes and Canceren_US
dc.rightsGenes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc.-
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCarcinoma, Hepatocellular - Geneticsen_US
dc.subject.meshChromosome Aberrations - Geneticsen_US
dc.subject.meshChromosome Deletionen_US
dc.subject.meshChromosome Disordersen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshHepatitis, Chronic - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshInterphase - Geneticsen_US
dc.subject.meshLiver Neoplasms - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.titleRecurrent chromosome alterations in hepatocellular carcinoma detected by comparative hybridizationen_US
dc.typeArticleen_US
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_US
dc.identifier.emailKwong, DLW:dlwkwong@hku.hken_US
dc.identifier.authorityGuan, XY=rp00454en_US
dc.identifier.authorityKwong, DLW=rp00414en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/1098-2264(2000)9999:9999<::AID-GCC1022>3.0.CO;2-V-
dc.identifier.pmid10959090en_US
dc.identifier.scopuseid_2-s2.0-0033843955en_US
dc.identifier.hkuros61908-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033843955&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume29en_US
dc.identifier.issue2en_US
dc.identifier.spage110en_US
dc.identifier.epage116en_US
dc.identifier.isiWOS:000089120300004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGuan, XY=7201463221en_US
dc.identifier.scopusauthoridFang, Y=7403457405en_US
dc.identifier.scopusauthoridSham, JST=7101655565en_US
dc.identifier.scopusauthoridKwong, DLW=15744231600en_US
dc.identifier.scopusauthoridZhang, Y=35202474200en_US
dc.identifier.scopusauthoridLiang, Q=7102360486en_US
dc.identifier.scopusauthoridLi, H=14420042900en_US
dc.identifier.scopusauthoridZhou, H=23104451800en_US
dc.identifier.scopusauthoridTrent, JM=7201692482en_US

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