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Article: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma

TitleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2008, v. 47 n. 2, p. 503-510 How to Cite?
AbstractAmplification of 1q21 is the most frequent genetic alteration in human hepatocellular carcinoma (HCC), being detected in 58%-78% of primary HCC cases by comparative genomic hybridization. Recently, we isolated a candidate oncogene, Amplified in Liver Cancer 1 (ALC1), from 1q21 by hybrid selection. Here we demonstrate that ALC1 was frequently amplified and overexpressed in HCC. ALC1-transfected cells possessed a strong oncogenic ability, increasing the colony formation in soft agar and increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against ALC1. Functional studies showed that overexpression of ALC1 could promote G1/S phase transition and inhibit apoptosis. Molecular studies revealed that the oncogenic function of ALC1 might be associated with its roles in promoting cell proliferation by down-regulating p53 expression. Conclusion: These results suggest that ALC1 is the target oncogene within the 1q21 amplicon and plays a pivotal role in HCC pathogenesis. Copyright © 2007 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/71967
ISSN
2014 Impact Factor: 11.055
2014 SCImago Journal Rankings: 4.310
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, NFen_HK
dc.contributor.authorHu, Len_HK
dc.contributor.authorFung, JMen_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorTang, DJen_HK
dc.contributor.authorFu, Len_HK
dc.contributor.authorWu, Zen_HK
dc.contributor.authorChen, Men_HK
dc.contributor.authorFang, Yen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-06T06:37:00Z-
dc.date.available2010-09-06T06:37:00Z-
dc.date.issued2008en_HK
dc.identifier.citationHepatology, 2008, v. 47 n. 2, p. 503-510en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71967-
dc.description.abstractAmplification of 1q21 is the most frequent genetic alteration in human hepatocellular carcinoma (HCC), being detected in 58%-78% of primary HCC cases by comparative genomic hybridization. Recently, we isolated a candidate oncogene, Amplified in Liver Cancer 1 (ALC1), from 1q21 by hybrid selection. Here we demonstrate that ALC1 was frequently amplified and overexpressed in HCC. ALC1-transfected cells possessed a strong oncogenic ability, increasing the colony formation in soft agar and increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against ALC1. Functional studies showed that overexpression of ALC1 could promote G1/S phase transition and inhibit apoptosis. Molecular studies revealed that the oncogenic function of ALC1 might be associated with its roles in promoting cell proliferation by down-regulating p53 expression. Conclusion: These results suggest that ALC1 is the target oncogene within the 1q21 amplicon and plays a pivotal role in HCC pathogenesis. Copyright © 2007 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - pathologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshChromosomes, Human, Pair 1en_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLiver Neoplasms - genetics - pathologyen_HK
dc.subject.meshOncogene Proteins - geneticsen_HK
dc.subject.meshOncogenesen_HK
dc.titleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=47&spage=503&epage=510&date=2008&atitle=Isolation+and+characterization+of+a+novel+oncogene,+amplified+in+liver+cancer+1,+within+a+commonly+amplified+region+at+1q21+in+hepatocellular+carcinoma.en_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailFu, L:gracelfu@hku.hken_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityFu, L=rp01435en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.22072en_HK
dc.identifier.pmid18023026-
dc.identifier.scopuseid_2-s2.0-39549087444en_HK
dc.identifier.hkuros146193en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39549087444&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue2en_HK
dc.identifier.spage503en_HK
dc.identifier.epage510en_HK
dc.identifier.isiWOS:000252939500019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMa, NF=35731661400en_HK
dc.identifier.scopusauthoridHu, L=34770075600en_HK
dc.identifier.scopusauthoridFung, JM=23469161200en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridChen, L=23569135400en_HK
dc.identifier.scopusauthoridTang, DJ=12752134500en_HK
dc.identifier.scopusauthoridFu, L=22979236700en_HK
dc.identifier.scopusauthoridWu, Z=8218909600en_HK
dc.identifier.scopusauthoridChen, M=13204327400en_HK
dc.identifier.scopusauthoridFang, Y=7403457405en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.citeulike2937519-

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