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Article: Clinicopathologic significance of genetic alterations in hepatocellular carcinoma

TitleClinicopathologic significance of genetic alterations in hepatocellular carcinoma
Authors
Issue Date2003
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2003, v. 146 n. 1, p. 8-15 How to Cite?
AbstractHepatocarcinogenesis may involve multiple mutations with distinctive pathogenetic and clinicopathologic significance. To test this hypothesis, 68 cases of hepatocellular carcinoma (HCC) were studied prospectively for genetic-clinicopathologic correlation. Ten pathologic characteristics were evaluated. TP53 (alias p53) gene mutation was studied by a polymerase chain reaction (PCR)-single-strand conformation polymorphism-sequencing; CDKN2B (alias p15) and CDKN2A (alias p16) gene methylation by methylation-specific PCR; and genetic imbalances by comparative genomic hybridization (CGH). TP53 gene mutations occurred in 25% of cases, more than half being codon 249 G to T transversion. Methylation of CDKN2A was frequent (61.7%); of CDKN2B, rare (5.9%). The CGH analysis showed a median of nine aberrations per case, with amplifications more frequent than deletions. Isochromosomes might be involved in about 25% of cases. Amplifications of 1q and 8q were most frequent. Clinicopathologic correlations showed that CDKN2A methylation was significantly associated with tumors arising in cirrhotic livers; amplifications of 17q was significant in multiple parameters of tumor invasiveness (size, venous invasion, poor cellular differentiation, microsatellite formation); other amplifications (1q, 6p, 10p, and 20p) were also significant in tumor invasion; and deletions (at 1p, 11q, 4q, and 14q) were significant in tumor growth. Consistent patterns of genetic alterations were defined in HCC, which might represent distinctive pathways in hepatocarcinogenesis. © 2003 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77847
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPang, Aen_HK
dc.contributor.authorNg, IOen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:36:23Z-
dc.date.available2010-09-06T07:36:23Z-
dc.date.issued2003en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2003, v. 146 n. 1, p. 8-15en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77847-
dc.description.abstractHepatocarcinogenesis may involve multiple mutations with distinctive pathogenetic and clinicopathologic significance. To test this hypothesis, 68 cases of hepatocellular carcinoma (HCC) were studied prospectively for genetic-clinicopathologic correlation. Ten pathologic characteristics were evaluated. TP53 (alias p53) gene mutation was studied by a polymerase chain reaction (PCR)-single-strand conformation polymorphism-sequencing; CDKN2B (alias p15) and CDKN2A (alias p16) gene methylation by methylation-specific PCR; and genetic imbalances by comparative genomic hybridization (CGH). TP53 gene mutations occurred in 25% of cases, more than half being codon 249 G to T transversion. Methylation of CDKN2A was frequent (61.7%); of CDKN2B, rare (5.9%). The CGH analysis showed a median of nine aberrations per case, with amplifications more frequent than deletions. Isochromosomes might be involved in about 25% of cases. Amplifications of 1q and 8q were most frequent. Clinicopathologic correlations showed that CDKN2A methylation was significantly associated with tumors arising in cirrhotic livers; amplifications of 17q was significant in multiple parameters of tumor invasiveness (size, venous invasion, poor cellular differentiation, microsatellite formation); other amplifications (1q, 6p, 10p, and 20p) were also significant in tumor invasion; and deletions (at 1p, 11q, 4q, and 14q) were significant in tumor growth. Consistent patterns of genetic alterations were defined in HCC, which might represent distinctive pathways in hepatocarcinogenesis. © 2003 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.en_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - metabolism - physiopathologyen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA, Neoplasm - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, p16en_HK
dc.subject.meshGenes, p53en_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Neoplasms - genetics - metabolism - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutationen_HK
dc.subject.meshNucleic Acid Hybridizationen_HK
dc.subject.meshProspective Studiesen_HK
dc.subject.meshSequence Deletionen_HK
dc.titleClinicopathologic significance of genetic alterations in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=146&issue=1&spage=8&epage=15&date=2003&atitle=Clinicopathologic+significance+of+genetic+alterations+in+hepatocellular+carcinomaen_HK
dc.identifier.emailNg, IO: iolng@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailKwong, YL: ylkwong@hku.hken_HK
dc.identifier.authorityNg, IO=rp00335en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0165-4608(03)00103-1en_HK
dc.identifier.pmid14499690-
dc.identifier.scopuseid_2-s2.0-0141453688en_HK
dc.identifier.hkuros90591en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0141453688&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume146en_HK
dc.identifier.issue1en_HK
dc.identifier.spage8en_HK
dc.identifier.epage15en_HK
dc.identifier.isiWOS:000185595100002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridPang, A=7007044165en_HK
dc.identifier.scopusauthoridNg, IO=7102753722en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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