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dc.contributor.authorPang, Dong
dc.contributor.authorAlston, Robert D
dc.contributor.authorEden, Tim O B
dc.contributor.authorBirch, Jillian M
dc.date.accessioned2009-04-01T23:09:57Z
dc.date.available2009-04-01T23:09:57Z
dc.date.issued2008-09-15
dc.identifier.citationCancer risks among relatives of children with Hodgkin and non-Hodgkin lymphoma. 2008, 123 (6):1407-10 Int. J. Canceren
dc.identifier.issn1097-0215
dc.identifier.pmid18561317
dc.identifier.doi10.1002/ijc.23651
dc.identifier.urihttp://hdl.handle.net/10541/58684
dc.description.abstractA role for genetic susceptibility in the aetiology of childhood lymphomas was investigated in 454 families of children with histologically confirmed Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL) from Northwest England. Cancers in parents were obtained from the UK National Health Service Central Register and in other close relatives by interview with the parents. The cancer incidence among relatives was compared with expected incidence based on cancer registry data for England. There were 197 cancers in relatives (SIR 1.0 95% CI 0.8-1.1). In families of children with HL, there was an excess of HL in the first degree relatives (SIR 5.8 95% CI 1.2-16.9). Excesses of HL diagnosed under population median age (SIR 4.1 95% CI 1.1-10.6) were seen among all relatives and relatives of children who were below the median age at diagnosis (SIR 5.5 95% CI 1.1-16.0). In families of children with NHL, there were non-significant excesses of central nervous system (CNS) tumours in the first degree relatives (SIR 2.9 95% CI 0.8-7.4) and in the second and third degree relatives (SIR 1.5). There were significant excesses of CNS tumours diagnosed under the population median age (SIR 2.8 95% CI 1.1-5.8) in all relatives. Excess CNS tumours were also seen among relatives of children below the median age at diagnosis (SIR 3.2 95% CI 1.1-7.6). In conclusion, genetic susceptibility in some families of children with lymphoma might be operating, but aetiologies in HL and NHL appear to be different. Possible interpretations of our findings, in the context of putative genetic and infectious aetiologies, are discussed.
dc.language.isoenen
dc.subjectFamilial Cancer Risken
dc.subjectCanceren
dc.subjectHodgkin Lymphomaen
dc.subjectCNS Tumouren
dc.subject.meshChild
dc.subject.meshFemale
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshHodgkin Disease
dc.subject.meshHumans
dc.subject.meshIncidence
dc.subject.meshLymphoma, Non-Hodgkin
dc.subject.meshMale
dc.subject.meshNeoplasms
dc.subject.meshPedigree
dc.subject.meshRegistries
dc.subject.meshRisk Factors
dc.titleCancer risks among relatives of children with Hodgkin and non-Hodgkin lymphoma.en
dc.typeArticleen
dc.contributor.departmentUniversity of Manchester and Cancer Research UK, Paediatric and Familial Cancer Research Group, Royal Manchester Children's Hospital, Manchester, United Kingdom. dong.pang@manchester.ac.uken
dc.identifier.journalInternational Journal of Canceren
html.description.abstractA role for genetic susceptibility in the aetiology of childhood lymphomas was investigated in 454 families of children with histologically confirmed Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL) from Northwest England. Cancers in parents were obtained from the UK National Health Service Central Register and in other close relatives by interview with the parents. The cancer incidence among relatives was compared with expected incidence based on cancer registry data for England. There were 197 cancers in relatives (SIR 1.0 95% CI 0.8-1.1). In families of children with HL, there was an excess of HL in the first degree relatives (SIR 5.8 95% CI 1.2-16.9). Excesses of HL diagnosed under population median age (SIR 4.1 95% CI 1.1-10.6) were seen among all relatives and relatives of children who were below the median age at diagnosis (SIR 5.5 95% CI 1.1-16.0). In families of children with NHL, there were non-significant excesses of central nervous system (CNS) tumours in the first degree relatives (SIR 2.9 95% CI 0.8-7.4) and in the second and third degree relatives (SIR 1.5). There were significant excesses of CNS tumours diagnosed under the population median age (SIR 2.8 95% CI 1.1-5.8) in all relatives. Excess CNS tumours were also seen among relatives of children below the median age at diagnosis (SIR 3.2 95% CI 1.1-7.6). In conclusion, genetic susceptibility in some families of children with lymphoma might be operating, but aetiologies in HL and NHL appear to be different. Possible interpretations of our findings, in the context of putative genetic and infectious aetiologies, are discussed.


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