Korczak J F, Pugh E W, Premkumar S, Guo X, Elston R C, Bailey-Wilson J E
Department of Biometry and Genetics, Louisiana State University Medical Center, New Orleans, USA.
Genet Epidemiol. 1995;12(6):625-30. doi: 10.1002/gepi.1370120617.
Model-free sib-pair linkage analysis was used to screen the GAW9-Problem 1 data set for evidence of linkage of a rare disease to any of 360 highly polymorphic marker loci. Negative regressions nominally significant at the alpha = 0.05 level were obtained for 44 markers; however all of these proved to be Type I errors. None of the four disease loci were detected by sib-pair linkage, which was not surprising, given the particular model and sampling scheme used to generate these data. Neither deleting parental marker genotypic information nor misspecifying marker allele frequency estimates substantially increased the Type I error rate. A two-stage testing procedure using a 10 or 20 cM map and a liberal first stage significance level gave the same overall results as a one-stage 2 cM map but required only about 42% or 22% as many markers, respectively.
采用无模型同胞对连锁分析方法，对GAW9问题1数据集进行筛查，以寻找一种罕见疾病与360个高度多态性标记位点中任何一个位点连锁的证据。在α = 0.05水平上名义上显著的负回归在44个标记中获得；然而，所有这些都被证明是I型错误。同胞对连锁未检测到四个疾病位点中的任何一个，鉴于用于生成这些数据的特定模型和抽样方案，这并不奇怪。删除亲本标记基因型信息或错误指定标记等位基因频率估计值均未显著增加I型错误率。使用10或20厘摩图谱以及宽松的第一阶段显著性水平的两阶段检验程序，与单阶段2厘摩图谱给出的总体结果相同，但分别只需要大约42%或22%的标记。
