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- Publisher Website: 10.1016/S0165-4608(02)00654-4
- Scopus: eid_2-s2.0-0037243435
- PMID: 12550757
- WOS: WOS:000180401900007
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Article: Evidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma
Title | Evidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma |
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Authors | |
Issue Date | 2003 |
Publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene |
Citation | Cancer Genetics And Cytogenetics, 2003, v. 140 n. 1, p. 45-48 How to Cite? |
Abstract | Loss 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. |
Persistent Identifier | http://hdl.handle.net/10722/150772 |
ISSN | 2012 Impact Factor: 1.929 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Guan, XY | en_US |
dc.contributor.author | Sham, JST | en_US |
dc.contributor.author | Tai, LS | en_US |
dc.contributor.author | Fang, Y | en_US |
dc.contributor.author | Li, H | en_US |
dc.contributor.author | Liang, Q | en_US |
dc.date.accessioned | 2012-06-26T06:10:09Z | - |
dc.date.available | 2012-06-26T06:10:09Z | - |
dc.date.issued | 2003 | en_US |
dc.identifier.citation | Cancer Genetics And Cytogenetics, 2003, v. 140 n. 1, p. 45-48 | en_US |
dc.identifier.issn | 0165-4608 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/150772 | - |
dc.description.abstract | Loss 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. | en_US |
dc.language | eng | en_US |
dc.publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene | en_US |
dc.relation.ispartof | Cancer Genetics and Cytogenetics | en_US |
dc.subject.mesh | Alleles | en_US |
dc.subject.mesh | Carcinoma, Hepatocellular - Genetics | en_US |
dc.subject.mesh | Cell Transformation, Neoplastic - Genetics | en_US |
dc.subject.mesh | China | en_US |
dc.subject.mesh | Chromosome Mapping | en_US |
dc.subject.mesh | Chromosomes, Human, Pair 17 - Genetics - Ultrastructure | en_US |
dc.subject.mesh | Genes, Tumor Suppressor | en_US |
dc.subject.mesh | Genes, P53 | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Liver Neoplasms - Genetics | en_US |
dc.subject.mesh | Loss Of Heterozygosity | en_US |
dc.subject.mesh | Polymerase Chain Reaction | en_US |
dc.subject.mesh | Polymorphism, Single-Stranded Conformational | en_US |
dc.title | Evidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma | en_US |
dc.type | Article | en_US |
dc.identifier.email | Guan, XY:xyguan@hkucc.hku.hk | en_US |
dc.identifier.authority | Guan, XY=rp00454 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/S0165-4608(02)00654-4 | en_US |
dc.identifier.pmid | 12550757 | - |
dc.identifier.scopus | eid_2-s2.0-0037243435 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0037243435&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 140 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 45 | en_US |
dc.identifier.epage | 48 | en_US |
dc.identifier.isi | WOS:000180401900007 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Guan, XY=7201463221 | en_US |
dc.identifier.scopusauthorid | Sham, JST=7101655565 | en_US |
dc.identifier.scopusauthorid | Tai, LS=7004457333 | en_US |
dc.identifier.scopusauthorid | Fang, Y=7403457405 | en_US |
dc.identifier.scopusauthorid | Li, H=26643419400 | en_US |
dc.identifier.scopusauthorid | Liang, Q=7102360486 | en_US |
dc.identifier.issnl | 0165-4608 | - |