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dc.contributor.authorMacInnis, RJen_US
dc.contributor.authorAntoniou, ACen_US
dc.contributor.authorEeles, RAen_US
dc.contributor.authorSeveri, Gen_US
dc.contributor.authorGuy, Men_US
dc.contributor.authorMcGuffog, Len_US
dc.contributor.authorHall, ALen_US
dc.contributor.authorO'Brien, LTen_US
dc.contributor.authorWilkinson, RAen_US
dc.contributor.authorDearnaley, DPen_US
dc.contributor.authorArdern-Jones, ATen_US
dc.contributor.authorHorwich, Aen_US
dc.contributor.authorKhoo, VSen_US
dc.contributor.authorParker, CCen_US
dc.contributor.authorHuddart, RAen_US
dc.contributor.authorMcCredie, MRen_US
dc.contributor.authorSmith, Cen_US
dc.contributor.authorSouthey, MCen_US
dc.contributor.authorStaples, MPen_US
dc.contributor.authorEnglish, DRen_US
dc.contributor.authorHopper, JLen_US
dc.contributor.authorGiles, GGen_US
dc.contributor.authorEaston, DFen_US
dc.date.accessioned2018-06-13T15:07:04Z
dc.date.issued2010-01en_US
dc.identifier.citationGenetic epidemiology, 2010, 34 (1), pp. 42 - 50en_US
dc.identifier.issn0741-0395en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1866
dc.identifier.eissn1098-2272en_US
dc.identifier.doi10.1002/gepi.20433en_US
dc.description.abstractFamilial aggregation of prostate cancer is likely to be due to multiple susceptibility loci, perhaps acting in conjunction with shared lifestyle risk factors. Models that assume a single mode of inheritance may be unrealistic. We analyzed genetic models of susceptibility to prostate cancer using segregation analysis of occurrence in families ascertained through population-based series totaling 4390 incident cases. We investigated major gene models (dominant, recessive, general, X-linked), polygenic models, and mixed models of susceptibility using the pedigree analysis software MENDEL. The hypergeometric model was used to approximate polygenic inheritance. The best-fitting model for the familial aggregation of prostate cancer was the mixed recessive model. The frequency of the susceptibility allele in the population was estimated to be 0.15 (95% confidence interval (CI) 0.11-0.20), with a relative risk for homozygote carriers of 94 (95% CI 46-192), and a polygenic standard deviation of 2.01 (95% CI 1.72-2.34). These analyses suggest that one or more genes having a strong recessively inherited effect on risk, as well as a number of genes with variants having small multiplicative effects on risk, may account for the genetic susceptibility to prostate cancer. The recessive component would predict the observed higher familial risk for siblings of cases than for fathers, but this could also be due to other factors such as shared lifestyle by siblings, targeted screening effects, and/or non-additive effects of one or more genes.en_US
dc.formatPrinten_US
dc.format.extent42 - 50en_US
dc.languageengen_US
dc.language.isoengen_US
dc.subjectHumansen_US
dc.subjectProstatic Neoplasmsen_US
dc.subjectGenetic Predisposition to Diseaseen_US
dc.subjectRisk Factorsen_US
dc.subjectCase-Control Studiesen_US
dc.subjectAdult Childrenen_US
dc.subjectFathersen_US
dc.subjectSiblingsen_US
dc.subjectGenetics, Populationen_US
dc.subjectGenes, Recessiveen_US
dc.subjectModels, Geneticen_US
dc.subjectAdulten_US
dc.subjectAgeden_US
dc.subjectAged, 80 and overen_US
dc.subjectMiddle Ageden_US
dc.subjectAustraliaen_US
dc.subjectMaleen_US
dc.subjectUnited Kingdomen_US
dc.titleProstate cancer segregation analyses using 4390 families from UK and Australian population-based studies.en_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1002/gepi.20433en_US
rioxxterms.licenseref.startdate2010-01en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfGenetic epidemiologyen_US
pubs.issue1en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Clinical Academic Radiotherapy (Dearnaley)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Oncogenetics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Radiotherapy and Imaging
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Radiotherapy and Imaging/Clinical Academic Radiotherapy (Huddart)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Radiotherapy and Imaging/Oncogenetics
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.publication-statusPublisheden_US
pubs.volume34en_US
pubs.embargo.termsNot knownen_US
icr.researchteamClinical Academic Radiotherapy (Dearnaley)en_US
icr.researchteamClinical Academic Radiotherapy (Huddart)en_US
icr.researchteamOncogeneticsen_US
dc.contributor.icrauthorDearnaley, Daviden_US
dc.contributor.icrauthorHorwich, Alanen_US
dc.contributor.icrauthorEeles, Rosalinden_US
dc.contributor.icrauthorHuddart, Roberten_US
dc.contributor.icrauthorParker, Chrisen_US
dc.contributor.icrauthorKhoo, Vincenten_US


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