Linkage analysis for ATM in familial B cell chronic lymphocytic leukaemia

被引:27
作者
Bevan, S
Catovsky, D
Marossy, A
Matutes, E
Popat, S
Antonovic, P
Bell, A
Berrebi, A
Gaminara, EJ
Quabeck, K
Ribeiro, I
Mauro, FR
Stark, P
Sykes, H
van Dongen, J
Wimperis, J
Wright, S
Yuille, MR [1 ]
Houlston, RS
机构
[1] Inst Canc Res, Acad Dept Haematol & Cytogenet, Surrey SN2 5NG, England
[2] Inst Canc Res, Sect Canc Genet, Surrey SN2 5NG, England
[3] Reg Sykenhuset Tromso, Tromso, Norway
[4] Poole Gen Hosp, Poole, Dorset, England
[5] Kaplan Med Ctr, Rehovot, Israel
[6] St Albans City Hosp, St Albans, England
[7] Facharzte Innere Med & Hamatol, Duisburg, Germany
[8] Hosp Egas Moniz, Lisbon, Portugal
[9] Univ La Sapienza, Rome, Italy
[10] Rabin Med Ctr, Petah Tiqva, Israel
[11] Kingston Gen Hosp, Surrey, England
[12] Erasmus Univ, Rotterdam, Netherlands
[13] Norfolk & Norwich Hosp, Norwich NR1 3SR, Norfolk, England
[14] Mater Misericordiae Hosp, S Brisbane, Australia
关键词
ATM; linkage; familial; chronic lymphocytic leukaemia; chromosome; 11q;
D O I
10.1038/sj.leu.2401531
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
B cell chronic lymphocytic leukaemia (CLL) shows evidence of familial aggregation, but the inherited basis is poorly understood. Mutations in the ATM gene have been demonstrated in CLL. This, coupled with a possibly increased risk of leukaemia in relatives of patients with Ataxia Telangiectasia, led us to question whether the ATM gene is involved in familial cases of CLL. To examine this proposition we typed five markers on chromosome 11q in 24 CLL families. No evidence for linkage between CLL and ATM in the 24 families studied and the best estimates of the proportion of sibling pairs that share no, one or both haplotypes at ATM were not different from their null expectations. This would imply that ATM is unlikely to make a significant contribution to the three-fold increase in risk of CLL seen in relatives of patients.
引用
收藏
页码:1497 / 1500
页数:4
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