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Article: Chromosome 1q21 amplification and oncogenes in hepatocellular carcinoma

TitleChromosome 1q21 amplification and oncogenes in hepatocellular carcinoma
Authors
Issue Date2010
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica, 2010, v. 31 n. 9, p. 1165-1171 How to Cite?
AbstractHepatocellular carcinoma (HCC) is among the most lethal of human malignancies. During human multistep hepatocarcinogenesis, genomic gain represents an important mechanism in the activation of proto-oncogenes. In many circumstances, activated oncogenes hold clinical implications both as prognostic markers and targets for cancer therapeutics. Gain of chromosome 1q copy is one of the most frequently detected alterations in HCC and 1q21 is the most frequent minimal amplifying region (MAR). A better understanding of the physiological and pathophysiological roles of target genes within 1q21 amplicon will significantly improve our knowledge in HCC pathogenesis, and may lead to a much more effective management of HCC bearing amplification of 1q21. Such knowledge has long term implications for the development of new therapeutic strategies for HCC treatment. Our research group and others, focused on the identification and characterization of 1q21 target genes such as JTB, CKS1B, and CHD1L in HCC progression. In this review, we will summarize the current scientific knowledge of known target genes within 1q21 amplicon and the precise oncogenic mechanisms of CHD1L will be discussed in detail. © 2010 CPS and SIMM All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/150832
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Len_US
dc.contributor.authorChan, THMen_US
dc.contributor.authorGuan, XYen_US
dc.date.accessioned2012-06-26T06:11:41Z-
dc.date.available2012-06-26T06:11:41Z-
dc.date.issued2010en_US
dc.identifier.citationActa Pharmacologica Sinica, 2010, v. 31 n. 9, p. 1165-1171en_US
dc.identifier.issn1671-4083en_US
dc.identifier.urihttp://hdl.handle.net/10722/150832-
dc.description.abstractHepatocellular carcinoma (HCC) is among the most lethal of human malignancies. During human multistep hepatocarcinogenesis, genomic gain represents an important mechanism in the activation of proto-oncogenes. In many circumstances, activated oncogenes hold clinical implications both as prognostic markers and targets for cancer therapeutics. Gain of chromosome 1q copy is one of the most frequently detected alterations in HCC and 1q21 is the most frequent minimal amplifying region (MAR). A better understanding of the physiological and pathophysiological roles of target genes within 1q21 amplicon will significantly improve our knowledge in HCC pathogenesis, and may lead to a much more effective management of HCC bearing amplification of 1q21. Such knowledge has long term implications for the development of new therapeutic strategies for HCC treatment. Our research group and others, focused on the identification and characterization of 1q21 target genes such as JTB, CKS1B, and CHD1L in HCC progression. In this review, we will summarize the current scientific knowledge of known target genes within 1q21 amplicon and the precise oncogenic mechanisms of CHD1L will be discussed in detail. © 2010 CPS and SIMM All rights reserved.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.htmlen_US
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCarcinoma, Hepatocellular - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 1en_US
dc.subject.meshDna Helicases - Geneticsen_US
dc.subject.meshDna-Binding Proteins - Geneticsen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshHumansen_US
dc.subject.meshOncogenesen_US
dc.titleChromosome 1q21 amplification and oncogenes in hepatocellular carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_US
dc.identifier.authorityGuan, XY=rp00454en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1038/aps.2010.94en_US
dc.identifier.pmid20676120-
dc.identifier.pmcidPMC4002324-
dc.identifier.scopuseid_2-s2.0-77956361953en_US
dc.identifier.hkuros183172-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956361953&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume31en_US
dc.identifier.issue9en_US
dc.identifier.spage1165en_US
dc.identifier.epage1171en_US
dc.identifier.isiWOS:000281562900023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChen, L=23569135400en_US
dc.identifier.scopusauthoridChan, THM=26431726400en_US
dc.identifier.scopusauthoridGuan, XY=7201463221en_US

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