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dc.contributor.authorBoyle, John M
dc.contributor.authorGreaves, Martin J
dc.contributor.authorCamplejohn, R S
dc.contributor.authorBirch, Jillian M
dc.contributor.authorRoberts, Stephen A
dc.contributor.authorVarley, Jennifer
dc.date.accessioned2010-01-20T15:53:23Z
dc.date.available2010-01-20T15:53:23Z
dc.date.issued1999-04
dc.identifier.citationRadiation-induced G1 arrest is not defective in fibroblasts from Li-Fraumeni families without TP53 mutations. 1999, 79 (11-12):1657-64 Br. J. Canceren
dc.identifier.issn0007-0920
dc.identifier.pmid10206274
dc.identifier.doi10.1038/sj.bjc.6690265
dc.identifier.urihttp://hdl.handle.net/10541/90157
dc.description.abstractRadiation-induced G1 arrest was studied in four classes of early passage skin fibroblasts comprising 12 normals, 12 heterozygous (mut/wt) TP53 mutation-carriers, two homozygous (mut/-) TP53 mutation-carriers and 16 strains from nine Li-Fraumeni syndrome or Li-Fraumeni-like families in which no TP53 mutation has been found, despite sequencing of all exons, exon-intron boundaries, 3' and 5' untranslated regions and promoter regions. In an assay of p53 allelic expression in yeast, cDNAs from these non-mutation strains behaved as wild-type p53. Using two different assays, we found G1 arrest was reduced in heterozygous strains with mis-sense mutations and one truncation mutation, when compared to the range established for the normal cells. Heterozygous strains with mutations at splice sites behaved like normal cells, whilst homozygous (mut/-) strains showed either extremely reduced, or no, arrest. Strains from all nine non-mutation families gave responses within the normal range. Exceptions to the previously reported inverse correlation between G1 arrest and clonogenic radiation resistance were observed, indicating that these phenotypes are not strictly interdependent.
dc.language.isoenen
dc.subject.meshAlleles
dc.subject.meshColony-Forming Units Assay
dc.subject.meshFibroblasts
dc.subject.meshG1 Phase
dc.subject.meshHeterozygote Detection
dc.subject.meshHumans
dc.subject.meshLi-Fraumeni Syndrome
dc.subject.meshMutation
dc.subject.meshSaccharomyces cerevisiae
dc.titleRadiation-induced G1 arrest is not defective in fibroblasts from Li-Fraumeni families without TP53 mutations.en
dc.typeArticleen
dc.contributor.departmentCRC Section of Molecular Genetics, Paterson Institute for Cancer Research, Christie CRC Research Centre, Manchester, UK.en
dc.identifier.journalBritish Journal of Canceren
html.description.abstractRadiation-induced G1 arrest was studied in four classes of early passage skin fibroblasts comprising 12 normals, 12 heterozygous (mut/wt) TP53 mutation-carriers, two homozygous (mut/-) TP53 mutation-carriers and 16 strains from nine Li-Fraumeni syndrome or Li-Fraumeni-like families in which no TP53 mutation has been found, despite sequencing of all exons, exon-intron boundaries, 3' and 5' untranslated regions and promoter regions. In an assay of p53 allelic expression in yeast, cDNAs from these non-mutation strains behaved as wild-type p53. Using two different assays, we found G1 arrest was reduced in heterozygous strains with mis-sense mutations and one truncation mutation, when compared to the range established for the normal cells. Heterozygous strains with mutations at splice sites behaved like normal cells, whilst homozygous (mut/-) strains showed either extremely reduced, or no, arrest. Strains from all nine non-mutation families gave responses within the normal range. Exceptions to the previously reported inverse correlation between G1 arrest and clonogenic radiation resistance were observed, indicating that these phenotypes are not strictly interdependent.


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