Table 2.
Method |
Discordant Sib-Pair |
Affected Sib-Pair |
Extended Pedigree |
Mixed Family Types |
||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
0%a | 25%a | 50%a | 0% | 25% | 50% | 0% | 25% | 50% | 0% | 25% | 50% | |
Epstein’s ASPb | – | – | – | 0.23 | 0.23 | 0.23 | – | – | – | 0.10 | 0.10 | 0.10 |
FBAT | 0.46 | 0.40 | 0.35 | 0.80 | 0.71 | 0.54 | 0.42 | 0.38 | 0.34 | 0.61 | 0.52 | 0.38 |
RV-PDT | 0.51 | 0.45 | 0.42 | 0.79 | 0.70 | 0.52 | 0.48 | 0.45 | 0.41 | 0.63 | 0.55 | 0.43 |
RV-GDT | 0.53 | 0.48 | 0.45 | 0.81 | 0.75 | 0.62 | 0.64 | 0.62 | 0.60 | 0.66 | 0.62 | 0.56 |
Genetic variant data were generated for 1,000 families of each pedigree structure shown in Figure 1 and mixed pedigree structures with the use of ExAC non-Finnish European variant information. Genotype data were generated for 17,987 autosomal genes across the genome when 75% of the rare nonsense, missense, and splice-site variants were randomly selected to be causal with an OR of 2.5, and power was evaluated as the proportion of genes with a p value < 0.05.
Probability that each founder is missing all genotype data.
Power was evaluated under the assumption that the exact IBD sharing between affected sib-pairs is known. Unknown IBD sharing and non-simulated data would reduce the power.