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Article: In vitro aflatoxin B1-induced p53 mutations

TitleIn vitro aflatoxin B1-induced p53 mutations
Authors
KeywordsAflatoxin B1
CpG dinucleotide
Hot spot mutation
Methylation
p53
Yeast p53 functional assay
Issue Date2003
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2003, v. 199 n. 1, p. 1-7 How to Cite?
AbstractThe tumor suppressor gene p53 is commonly mutated with high frequencies at certain hot spots in human cancers. In liver cancers there is an especially high frequency of mutations at codon 249. To study the impact of carcinogen targeting and the role of cytosine methylation on the mutation spectrum, a common liver cancer carcinogen aflatoxin B1 (AFB1), was studied using the p53 cDNA template to examine mutation induction. Subsequent mutations were detected with a yeast p53 functional assay and identified by DNA sequencing. The results indicated that cytosine methylation enhances AFB1-induced guanine mutations at CpG sites. However, no mutations were detected at codon 249. © 2003 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/150778
ISSN
2023 Impact Factor: 9.1
2023 SCImago Journal Rankings: 2.595
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, KTen_US
dc.contributor.authorHsientang Hsieh, DPen_US
dc.contributor.authorLung, MLen_US
dc.date.accessioned2012-06-26T06:10:19Z-
dc.date.available2012-06-26T06:10:19Z-
dc.date.issued2003en_US
dc.identifier.citationCancer Letters, 2003, v. 199 n. 1, p. 1-7en_US
dc.identifier.issn0304-3835en_US
dc.identifier.urihttp://hdl.handle.net/10722/150778-
dc.description.abstractThe tumor suppressor gene p53 is commonly mutated with high frequencies at certain hot spots in human cancers. In liver cancers there is an especially high frequency of mutations at codon 249. To study the impact of carcinogen targeting and the role of cytosine methylation on the mutation spectrum, a common liver cancer carcinogen aflatoxin B1 (AFB1), was studied using the p53 cDNA template to examine mutation induction. Subsequent mutations were detected with a yeast p53 functional assay and identified by DNA sequencing. The results indicated that cytosine methylation enhances AFB1-induced guanine mutations at CpG sites. However, no mutations were detected at codon 249. © 2003 Elsevier Ireland Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_US
dc.relation.ispartofCancer Lettersen_US
dc.subjectAflatoxin B1-
dc.subjectCpG dinucleotide-
dc.subjectHot spot mutation-
dc.subjectMethylation-
dc.subjectp53-
dc.subjectYeast p53 functional assay-
dc.subject.meshAflatoxin B1 - Toxicityen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCarcinogensen_US
dc.subject.meshCodon - Geneticsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDna, Complementaryen_US
dc.subject.meshDinucleoside Phosphates - Metabolismen_US
dc.subject.meshGenes, P53 - Drug Effectsen_US
dc.subject.meshMutagensen_US
dc.subject.meshPlasmids - Drug Effects - Geneticsen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshSaccharomyces Cerevisiae - Drug Effects - Geneticsen_US
dc.subject.meshTemplates, Geneticen_US
dc.titleIn vitro aflatoxin B1-induced p53 mutationsen_US
dc.typeArticleen_US
dc.identifier.emailLung, ML:mlilung@hku.hken_US
dc.identifier.authorityLung, ML=rp00300en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0304-3835(03)00337-9en_US
dc.identifier.pmid12963117-
dc.identifier.scopuseid_2-s2.0-0041732392en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0041732392&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume199en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage7en_US
dc.identifier.isiWOS:000185528200001-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridChan, KT=7406034062en_US
dc.identifier.scopusauthoridHsientang Hsieh, DP=6504331460en_US
dc.identifier.scopusauthoridLung, ML=7006411788en_US
dc.identifier.issnl0304-3835-

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