Cancer risks among relatives of children with Hodgkin and non-Hodgkin lymphoma

被引:13
|
作者
Pang, Dong [1 ]
Alston, Robert D. [1 ]
Eden, Tim O. B. [2 ]
Birch, Jillian M. [1 ]
机构
[1] Royal Manchester Childrens Hosp, Canc Res UK, Paediat & Familial Canc Res Grp, Manchester M27 4HA, Lancs, England
[2] Univ Manchester, Acad Unit Paediat Oncol, Christie Hosp NHS Trust, Teenage Canc Trust Oncol Unit, Manchester, Lancs, England
关键词
familial cancer risk; children; Hodgkin lymphoma; non-Hodgkin lymphoma; CNS tumour; population-based;
D O I
10.1002/ijc.23651
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A 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 front the UK National Health Service Central Register and in other close relatives by interview with the parents. e cancer incidence among relatives was compared with expecte 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 HI, diagnosed under population median age (SIR 4.195% 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 tinder 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. (C) 2008 Wiley-Liss, Inc.
引用
收藏
页码:1407 / 1410
页数:4
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