ArticleAmerican journal of human genetics2000
Comparison of tests for association and linkage in incomplete families.
Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Role of recombination and faithfulness to partner in sex chromosome degeneration.Scientific reports · 2018Article
- Handling missing data in transmission disequilibrium test in nuclear families with one affected offspring.PloS one · 2012Article
- Evolutionary contributions to solving the "matrilineal puzzle": a test of Holden, Sear, and Mace's model.Human nature (Hawthorne, N.Y.) · 2011Article
- Review and evaluation of methods correcting for population stratification with a focus on underlying statistical principles.Human heredity · 2008Review
- Haplotype thinking in lung disease.Proceedings of the American Thoracic Society · 2007Review
- Pooled association genome scanning for alcohol dependence using 104,268 SNPs: validation and use to identify alcoholism vulnerability loci in unrelated individuals from the collaborative study on the genetics of alcoholism.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2006Article
- Common variations in ALG9 are not associated with bipolar I disorder: a family-based study.Behavioral and brain functions : BBF · 2006Article
- SUP: an extension to SLINK to allow a larger number of marker loci to be simulated in pedigrees conditional on trait values.BMC genetics · 2006Article
- Pooled association genome scanning: validation and use to identify addiction vulnerability loci in two samples.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- No association between E- and L-selectin genes and SLE: soluble L-selectin levels do correlate with genotype and a subset in SLE.Genes and immunity · 2005Article
- Linkage of the dopamine receptor D1 gene to attention-deficit/hyperactivity disorder.Molecular psychiatry · 2004Article
- Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus.Human molecular genetics · 2004Article
- Informative missingness in genetic association studies: case-parent designs.American journal of human genetics · 2003Article
- Genetic variation in the 6p22.3 gene DTNBP1, the human ortholog of the mouse dysbindin gene, is associated with schizophrenia.American journal of human genetics · 2002Article
- Polysubstance abuse-vulnerability genes: genome scans for association, using 1,004 subjects and 1,494 single-nucleotide polymorphisms.American journal of human genetics · 2001Article
- Transmission/disequilibrium test meets measured haplotype analysis: family-based association analysis guided by evolution of haplotypes.American journal of human genetics · 2001Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To analyze incomplete families, the following statistical tests can be used: LRAT-a simple likelihood-based association test, TRANSMIT, SIBASSOC/STDT, and RCTDT. We compared these four tests, for the diallelic case, on simulated data sets. The comparisons focused on the power to detect linkage and association when different familial structures, resistance to population stratification, resistance to misclassification of the disease status of the healthy sib, and the effect of nonpaternity were considered. The simulations lead to the following conclusions. The type I errors of TRANSMIT, SIBASSOC/STDT, and RCTDT were not affected by population stratification. LRAT showed bias under strong population stratification. High nonpaternity rates can lead to inflated type I errors, highlighting the importance of identification of half sibs. Under different homogeneous models, the power of TRANSMIT was very similar to that of LRAT, and, similarly, no difference in power was observed between SIBASSOC/STDT and RCTDT. Under various recessive and additive models, TRANSMIT was slightly more powerful than SIBASSOC/STDT when monoparental families with one affected and one unaffected sib were analyzed. Under various dominant models, SIBASSOC/STDT was slightly more powerful than TRANSMIT. Misclassification of the disease status of healthy sibs, as well as the discarding of incomplete families, resulted in a consistent loss of power.
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