Article: Evidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma

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TitleEvidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma
AuthorsGuan, XY1
Sham, JST1
Tai, LS1
Fang, Y2
Li, H1
Liang, Q2
Issue Date2003
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
CitationCancer Genetics And Cytogenetics, 2003, v. 140 n. 1, p. 45-48 [How to Cite?]
DOI: http://dx.doi.org/10.1016/S0165-4608(02)00654-4
AbstractLoss of 17p is one of the most frequent chromosomal alterations in primary hepatocellular carcinoma (HCC). In the present study, the association between loss of 17p and TP53 mutation was analyzed in 94 primary HCC of Chinese patients. Loss of one allele at 17p13.3 distal to the TP53 gene was observed in 48 of 94 HCC (51%), whereas loss of heterozygosity (LOH) at 17p13.1 near the TP53 gene was detected in 30 of 94 HCC (32%) and TP53 mutation was detected in only 22 of 94 HCC (23%). High frequency of LOH at 17p13.3 and relatively low frequency of TP53 mutation in the present study indicate that loss of function of a putative tumor suppressor gene at 17p13.3 may play a more important role than TP53 in HCC development. © 2003 Elsevier Science Inc. All rights reserved.
ISSN0165-4608
2011 Impact Factor: 1.389
2011 SCImago Journal Rankings: 0.162
DOIhttp://dx.doi.org/10.1016/S0165-4608(02)00654-4
ISI Accession Number IDWOS:000180401900007
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorGuan, XY
dc.contributor.authorSham, JST
dc.contributor.authorTai, LS
dc.contributor.authorFang, Y
dc.contributor.authorLi, H
dc.contributor.authorLiang, Q
dc.date.accessioned2012-06-26T06:10:09Z
dc.date.available2012-06-26T06:10:09Z
dc.date.issued2003
dc.description.abstractLoss of 17p is one of the most frequent chromosomal alterations in primary hepatocellular carcinoma (HCC). In the present study, the association between loss of 17p and TP53 mutation was analyzed in 94 primary HCC of Chinese patients. Loss of one allele at 17p13.3 distal to the TP53 gene was observed in 48 of 94 HCC (51%), whereas loss of heterozygosity (LOH) at 17p13.1 near the TP53 gene was detected in 30 of 94 HCC (32%) and TP53 mutation was detected in only 22 of 94 HCC (23%). High frequency of LOH at 17p13.3 and relatively low frequency of TP53 mutation in the present study indicate that loss of function of a putative tumor suppressor gene at 17p13.3 may play a more important role than TP53 in HCC development. © 2003 Elsevier Science Inc. All rights reserved.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCancer Genetics And Cytogenetics, 2003, v. 140 n. 1, p. 45-48 [How to Cite?]
DOI: http://dx.doi.org/10.1016/S0165-4608(02)00654-4
dc.identifier.doihttp://dx.doi.org/10.1016/S0165-4608(02)00654-4
dc.identifier.epage48
dc.identifier.isiWOS:000180401900007
dc.identifier.issn0165-4608
2011 Impact Factor: 1.389
2011 SCImago Journal Rankings: 0.162
dc.identifier.issue1
dc.identifier.pmid12550757
dc.identifier.scopuseid_2-s2.0-0037243435
dc.identifier.spage45
dc.identifier.urihttp://hdl.handle.net/10722/150772
dc.identifier.volume140
dc.languageeng
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
dc.publisher.placeUnited States
dc.relation.ispartofCancer Genetics and Cytogenetics
dc.relation.referencesReferences in Scopus
dc.subject.meshAlleles
dc.subject.meshCarcinoma, Hepatocellular - Genetics
dc.subject.meshCell Transformation, Neoplastic - Genetics
dc.subject.meshChina
dc.subject.meshChromosome Mapping
dc.subject.meshChromosomes, Human, Pair 17 - Genetics - Ultrastructure
dc.subject.meshGenes, Tumor Suppressor
dc.subject.meshGenes, P53
dc.subject.meshHumans
dc.subject.meshLiver Neoplasms - Genetics
dc.subject.meshLoss Of Heterozygosity
dc.subject.meshPolymerase Chain Reaction
dc.subject.meshPolymorphism, Single-Stranded Conformational
dc.titleEvidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat Sen University of Medical Sciences