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Article: Hepatitis B virus-associated multistep hepatocarcinogenesis: A stepwise increase in allelic alterations

TitleHepatitis B virus-associated multistep hepatocarcinogenesis: A stepwise increase in allelic alterations
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2008, v. 68 n. 14, p. 5988-5996 How to Cite?
AbstractHepatocarcinogenesis is a multistep process, but systematic analysis using a genetic or molecular approach to accurately delineate the different stages of hepatocellular carcinoma (HCC) development is scarce. In this study, we used genomewide allelotyping to systematically evaluate the allelic alterations in the multisteps of hepatitis B virus-associated hepatocarcinogenesis. The overall fractional allelic loss (FAL) indices of cirrhosis, dysplastic nodules (DN), and HCC were significantly different, with a clear stepwise increase (P < 0.001). Loss of heterozygosity (LOH) was uncommon in cirrhotic livers (n = 24; mean FAL index ± SD, 0.09 ± 0.09; median, 0.07). In contrast, LOH was common in our 74 HCC nodules, which were predominantly hepatitis B virus-associated (mean FAL index ± SD, 0.40 ± 0.23; median, 0.38). The 18 DNs had FAL index (mean ± SD, 0.27 ± 0.19; median, 0.20) in between that of cirrhosis and HCC. Importantly, high-grade DNs had FAL index significantly higher than that of low-grade DNs (P = 0.031) and close to that of HCC, indicating that high-grade DNs were genetically closer to HCC. However, there was no significant difference in FAL indices between primary HCCs and their corresponding intrahepatic metastases, but this absence of major allelic losses in this transformation to a metastatic phenotype does not exclude small-scale chromosomal losses or gene deletions. To conclude, hepatitis B virus-associated hepatocarcinogenesis is a multistep process accompanied by stepwise increase in allelic losses from cirrhosis and low- and high-grade DN to HCC. Such allelic losses contribute to promote tumor development and progression. ©2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/60576
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, JMFen_HK
dc.contributor.authorWong, CMen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-05-31T04:14:00Z-
dc.date.available2010-05-31T04:14:00Z-
dc.date.issued2008en_HK
dc.identifier.citationCancer Research, 2008, v. 68 n. 14, p. 5988-5996en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60576-
dc.description.abstractHepatocarcinogenesis is a multistep process, but systematic analysis using a genetic or molecular approach to accurately delineate the different stages of hepatocellular carcinoma (HCC) development is scarce. In this study, we used genomewide allelotyping to systematically evaluate the allelic alterations in the multisteps of hepatitis B virus-associated hepatocarcinogenesis. The overall fractional allelic loss (FAL) indices of cirrhosis, dysplastic nodules (DN), and HCC were significantly different, with a clear stepwise increase (P < 0.001). Loss of heterozygosity (LOH) was uncommon in cirrhotic livers (n = 24; mean FAL index ± SD, 0.09 ± 0.09; median, 0.07). In contrast, LOH was common in our 74 HCC nodules, which were predominantly hepatitis B virus-associated (mean FAL index ± SD, 0.40 ± 0.23; median, 0.38). The 18 DNs had FAL index (mean ± SD, 0.27 ± 0.19; median, 0.20) in between that of cirrhosis and HCC. Importantly, high-grade DNs had FAL index significantly higher than that of low-grade DNs (P = 0.031) and close to that of HCC, indicating that high-grade DNs were genetically closer to HCC. However, there was no significant difference in FAL indices between primary HCCs and their corresponding intrahepatic metastases, but this absence of major allelic losses in this transformation to a metastatic phenotype does not exclude small-scale chromosomal losses or gene deletions. To conclude, hepatitis B virus-associated hepatocarcinogenesis is a multistep process accompanied by stepwise increase in allelic losses from cirrhosis and low- and high-grade DN to HCC. Such allelic losses contribute to promote tumor development and progression. ©2008 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAdulten_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - virologyen_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFibrosis - geneticsen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHepatitis B virus - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Neoplasms - genetics - virologyen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutationen_HK
dc.subject.meshNeoplasm Metastasisen_HK
dc.titleHepatitis B virus-associated multistep hepatocarcinogenesis: A stepwise increase in allelic alterationsen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, CM:jackwong@pathology.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityWong, CM=rp00231en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-08-0905en_HK
dc.identifier.pmid18632655-
dc.identifier.scopuseid_2-s2.0-48649088986en_HK
dc.identifier.hkuros146901en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48649088986&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume68en_HK
dc.identifier.issue14en_HK
dc.identifier.spage5988en_HK
dc.identifier.epage5996en_HK
dc.identifier.eissn1538-7445-
dc.identifier.isiWOS:000257768300059-
dc.publisher.placeUnited Statesen_HK

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