Please use this identifier to cite or link to this item: https://doi.org/10.1038/aps.2010.94
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dc.titleChromosome 1q21 amplification and oncogenes in hepatocellular carcinoma
dc.contributor.authorChen, L
dc.contributor.authorChan, T.H.M
dc.contributor.authorGuan, X.-Y
dc.date.accessioned2020-10-20T08:18:50Z
dc.date.available2020-10-20T08:18:50Z
dc.date.issued2010
dc.identifier.citationChen, L, Chan, T.H.M, Guan, X.-Y (2010). Chromosome 1q21 amplification and oncogenes in hepatocellular carcinoma. Acta Pharmacologica Sinica 31 (9) : 1165-1171. ScholarBank@NUS Repository. https://doi.org/10.1038/aps.2010.94
dc.identifier.issn1671-4083
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/178197
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.
dc.publisherWiley
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectcaspase 3
dc.subjectcaspase 9
dc.subjectcyclic AMP dependent protein kinase regulatory subunit Ibeta
dc.subjectcyclic AMP responsive element binding protein
dc.subjectamplicon
dc.subjectapoptosis
dc.subjectbinding affinity
dc.subjectcancer growth
dc.subjectcancer therapy
dc.subjectcell cycle progression
dc.subjectcell cycle regulation
dc.subjectcell proliferation
dc.subjectchromosome 13q
dc.subjectchromosome 16p
dc.subjectchromosome 17p
dc.subjectchromosome 17q
dc.subjectchromosome 1q
dc.subjectchromosome 20q
dc.subjectchromosome 4q
dc.subjectchromosome 6q
dc.subjectchromosome 8p
dc.subjectchromosome aberration
dc.subjectcomparative genomic hybridization
dc.subjectcopy number variation
dc.subjectdistant metastasis
dc.subjectdrug inhibition
dc.subjectgene amplification
dc.subjectgene loss
dc.subjectgene overexpression
dc.subjectgene targeting
dc.subjectgene translocation
dc.subjectgenetic gain
dc.subjectgenetic transfection
dc.subjecthuman
dc.subjectliver carcinogenesis
dc.subjectliver cell carcinoma
dc.subjectminimal amplified region
dc.subjectnonhuman
dc.subjectoncogene
dc.subjectreal time polymerase chain reaction
dc.subjectreview
dc.subjectsingle nucleotide polymorphism
dc.subjectAnimals
dc.subjectCarcinoma, Hepatocellular
dc.subjectChromosomes, Human, Pair 1
dc.subjectDNA Helicases
dc.subjectDNA-Binding Proteins
dc.subjectGene Amplification
dc.subjectHumans
dc.subjectOncogenes
dc.typeReview
dc.contributor.departmentANATOMY
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1038/aps.2010.94
dc.description.sourcetitleActa Pharmacologica Sinica
dc.description.volume31
dc.description.issue9
dc.description.page1165-1171
dc.published.statepublished
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