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Article: Molecular and functional genetics of hepatocellular carcinoma.

TitleMolecular and functional genetics of hepatocellular carcinoma.
Authors
Issue Date2010
Citation
Frontiers In Bioscience (Scholar Edition), 2010, v. 2, p. 117-134 How to Cite?
AbstractHepatocellular carcinoma (HCC) is the fifth most common cancer and one of the leading causes of cancer death worldwide. Hepatocarcinogenesis is a multistep process developing from normal through chronic hepatitis/cirrhosis and dysplastic nodules to HCC. Although we have insufficient understanding to propose a robust general model, with advances in molecular methods, there is a growing understanding of the molecular mechanisms in the development of HCC. Hepatocarcinogenesis is strongly linked to increases in allelic losses, chromosomal changes, gene mutations, epigenetic alterations, and alterations in molecular cellular pathways. Special emphasis in this review is given to the genetics, epigenetics, and regulation of major signaling pathways involved in HCC such as Wnt/b-catenin, Ras, and PI3K/Akt/mTOR pathways. A detailed understanding of the underlying molecular mechanisms involved in the progression of HCC can improve our prevention and diagnostic tools for HCC and be an important potential source of novel molecular targets for new therapies.
Persistent Identifierhttp://hdl.handle.net/10722/148624
ISSN
2015 SCImago Journal Rankings: 1.035

 

DC FieldValueLanguage
dc.contributor.authorYam, JWen_US
dc.contributor.authorWong, CMen_US
dc.contributor.authorNg, IOen_US
dc.date.accessioned2012-05-29T06:14:10Z-
dc.date.available2012-05-29T06:14:10Z-
dc.date.issued2010en_US
dc.identifier.citationFrontiers In Bioscience (Scholar Edition), 2010, v. 2, p. 117-134en_US
dc.identifier.issn1945-0524en_US
dc.identifier.urihttp://hdl.handle.net/10722/148624-
dc.description.abstractHepatocellular carcinoma (HCC) is the fifth most common cancer and one of the leading causes of cancer death worldwide. Hepatocarcinogenesis is a multistep process developing from normal through chronic hepatitis/cirrhosis and dysplastic nodules to HCC. Although we have insufficient understanding to propose a robust general model, with advances in molecular methods, there is a growing understanding of the molecular mechanisms in the development of HCC. Hepatocarcinogenesis is strongly linked to increases in allelic losses, chromosomal changes, gene mutations, epigenetic alterations, and alterations in molecular cellular pathways. Special emphasis in this review is given to the genetics, epigenetics, and regulation of major signaling pathways involved in HCC such as Wnt/b-catenin, Ras, and PI3K/Akt/mTOR pathways. A detailed understanding of the underlying molecular mechanisms involved in the progression of HCC can improve our prevention and diagnostic tools for HCC and be an important potential source of novel molecular targets for new therapies.en_US
dc.languageengen_US
dc.relation.ispartofFrontiers in bioscience (Scholar edition)en_US
dc.subject.meshAnimalsen_US
dc.subject.meshCarcinoma, Hepatocellular - Genetics - Physiopathologyen_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshEpigenesis, Geneticen_US
dc.subject.meshHumansen_US
dc.subject.meshIntracellular Signaling Peptides And Proteins - Metabolismen_US
dc.subject.meshLiver Neoplasms - Genetics - Physiopathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMutation - Geneticsen_US
dc.subject.meshP-Glycoproteins - Geneticsen_US
dc.subject.meshPhosphatidylinositol 3-Kinases - Metabolismen_US
dc.subject.meshPolymorphism, Single Nucleotideen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolismen_US
dc.subject.meshSignal Transduction - Genetics - Physiologyen_US
dc.subject.meshTor Serine-Threonine Kinasesen_US
dc.subject.meshWnt Proteins - Metabolismen_US
dc.subject.meshBeta Catenin - Metabolismen_US
dc.subject.meshRas Proteins - Metabolismen_US
dc.titleMolecular and functional genetics of hepatocellular carcinoma.en_US
dc.typeArticleen_US
dc.identifier.emailYam, JW:judyyam@pathology.hku.hken_US
dc.identifier.emailWong, CM:jackwong@pathology.hku.hken_US
dc.identifier.emailNg, IO:iolng@hkucc.hku.hken_US
dc.identifier.authorityYam, JW=rp00468en_US
dc.identifier.authorityWong, CM=rp00231en_US
dc.identifier.authorityNg, IO=rp00335en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid20036934-
dc.identifier.scopuseid_2-s2.0-77954119208en_US
dc.identifier.hkuros171419-
dc.identifier.volume2en_US
dc.identifier.spage117en_US
dc.identifier.epage134en_US

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