Genome-wide meta-analysis for rheumatoid arthritis
Genome-wide meta-analysis for rheumatoid arthritis
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DOI：
10.1007/s00439-006-0171-8
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发表时间：
2006-07-01
期刊：
影响因子：
5.3
通讯作者：
Amos, Christopher I.
中科院分区：
文献类型：
--
作者：
Etzel, Carol J.;Chen, Wei V.;Amos, Christopher I.
荟萃分析越来越多地被用作整合来自复杂表型的不同研究的数据的工具，因为任何一项研究识别因果位点的能力都是有限的。我们应用了一种新的荟萃分析方法（Loesgen 等人，Genet Epidemiol 21(Suppl 1):S142-S147, 2001）来编译四项关于白种人类风湿关节炎的研究结果，其中包括 NARAC 的两项研究（Jawaheer 等人，Am J Hum Genet 68:927-936, 2001；Jawaheer 等人，2001 年）。 Arthritis Rheum 48:906-916, 2003），一项来自英国的研究（MacKay 等人，Arthritis Rheum 46:632-639, 2001）和一项来自法国的研究（Cornelis 等人，Proc Natl Acad Sci USA 95:10746-10750, 1998）。对于每项研究，我们通过使用 GeneHunter2 进行区间作图（2 cM 区间）来获得 NPL 分数（Kruglyak 等人，Am J Hum Genet 58：1347-1363，1996；Markianos 等人，Am J Hum Genet 68：963-977，2001）。三个联合体组之间的标记图谱不同，因此，在完成间隔映射后对标记图谱进行对齐，并使用Loesgen等人的方法合并彼此在1 cM以内的NPL评分。 (Genet Epidemiol 21(Suppl 1):S142-S147, 2001)通过计算NPL分数的加权平均值。这种方法避免了在使用 GeneHunter2 进行分析时，当样品中的某些标记未进行基因分型时遇到的一些问题。该程序提供了 1、2、5 和 18 号染色体上连锁的边际证据 (P < 0.05)，8 号和 16 号染色体上的有力证据 (P < 0.01)，以及 6 号染色体 HLA 区域的压倒性证据。
Meta-analysis is being increasingly used as a tool for integrating data from different studies of complex phenotypes, because the power of any one study to identify causal loci is limited. We applied a novel meta-analytical approach (Loesgen et al. in Genet Epidemiol 21(Suppl 1):S142-S147, 2001) in compiling results from four studies of rheumatoid arthritis in Caucasians including two studies from NARAC (Jawaheer et al. in Am J Hum Genet 68:927-936, 2001; Jawaheer et al. in Arthritis Rheum 48:906-916, 2003), one study from the UK (MacKay et al. in Arthritis Rheum 46:632-639, 2001) and one from France (Cornelis et al. in Proc Natl Acad Sci USA 95:10746-10750, 1998). For each study, we obtained NPL scores by performing interval mapping (2 cM intervals) using GeneHunter2 (Kruglyak et al. in Am J Hum Genet 58:1347-1363, 1996; Markianos et al. in Am J Hum Genet 68:963-977, 2001). The marker maps differed among the three consortium groups, therefore, the marker maps were aligned after the interval mapping was completed and the NPL scores that were within 1 cM of each other were combined using the method of Loesgen et al. (Genet Epidemiol 21(Suppl 1):S142-S147, 2001) by calculating the weighted average of the NPL score. This approach avoids some problems in analysis encountered by using GeneHunter2 when some markers in the sample are not genotyped. This procedure provided marginal evidence (P < 0.05) of linkage on chromosome 1, 2, 5 and 18, strong evidence (P < 0.01) on chromosomes 8 and 16, and overwhelming evidence in the HLA region of chromosome 6.