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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
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TitleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
 
AuthorsMa, NF1 4
Hu, L1
Fung, JM1
Xie, D2
Zheng, BJ1
Chen, L1
Tang, DJ1
Fu, L1
Wu, Z3
Chen, M1
Fang, Y2
Guan, XY1 2
 
Issue Date2008
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
 
CitationHepatology, 2008, v. 47 n. 2, p. 503-510 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.22072
 
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.
 
ISSN0270-9139
2013 Impact Factor: 11.190
 
DOIhttp://dx.doi.org/10.1002/hep.22072
 
ISI Accession Number IDWOS:000252939500019
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorMa, NF
 
dc.contributor.authorHu, L
 
dc.contributor.authorFung, JM
 
dc.contributor.authorXie, D
 
dc.contributor.authorZheng, BJ
 
dc.contributor.authorChen, L
 
dc.contributor.authorTang, DJ
 
dc.contributor.authorFu, L
 
dc.contributor.authorWu, Z
 
dc.contributor.authorChen, M
 
dc.contributor.authorFang, Y
 
dc.contributor.authorGuan, XY
 
dc.date.accessioned2010-09-06T06:37:00Z
 
dc.date.available2010-09-06T06:37:00Z
 
dc.date.issued2008
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationHepatology, 2008, v. 47 n. 2, p. 503-510 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.22072
 
dc.identifier.citeulike2937519
 
dc.identifier.doihttp://dx.doi.org/10.1002/hep.22072
 
dc.identifier.epage510
 
dc.identifier.hkuros146193
 
dc.identifier.isiWOS:000252939500019
 
dc.identifier.issn0270-9139
2013 Impact Factor: 11.190
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid18023026
 
dc.identifier.scopuseid_2-s2.0-39549087444
 
dc.identifier.spage503
 
dc.identifier.urihttp://hdl.handle.net/10722/71967
 
dc.identifier.volume47
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofHepatology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshCarcinoma, Hepatocellular - genetics - pathology
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshChromosomes, Human, Pair 1
 
dc.subject.meshGene Amplification
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshGene Silencing
 
dc.subject.meshHumans
 
dc.subject.meshIn Situ Hybridization, Fluorescence
 
dc.subject.meshLiver Neoplasms - genetics - pathology
 
dc.subject.meshOncogene Proteins - genetics
 
dc.subject.meshOncogenes
 
dc.titleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
 
dc.typeArticle
 
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<description.abstract>Amplification 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 &#169; 2007 by the American Association for the Study of Liver Diseases.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat-Sen University
  3. Hong Kong University of Science and Technology
  4. Guangzhou Medical College