ArticleGenetic epidemiology2012
Identifying plausible genetic models based on association and linkage results: application to type 2 diabetes.
Article in Genetic epidemiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- The effect of FTO gene rs9939609 polymorphism on the association between colorectal cancer and different types of dietary fat intake: a case-control study.Journal of physiological anthropology · 2023Article
- Genotype imputation in case-only studies of gene-environment interaction: validity and power.Human genetics · 2021Article
- Robust and Powerful Affected Sibpair Test for Rare Variant Association.Genetic epidemiology · 2015Article
- Evaluating empirical bounds on complex disease genetic architecture.Nature genetics · 2013Article
- What will diabetes genomes tell us?Current diabetes reports · 2012Review
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Authors and funding
5 authors.
Funding
Abstract
When planning resequencing studies for complex diseases, previous association and linkage studies can constrain the range of plausible genetic models for a given locus. Here, we explore the combinations of causal risk allele frequency (RAFC ) and genotype relative risk (GRRC ) consistent with no or limited evidence for affected sibling pair (ASP) linkage and strong evidence for case-control association. We find that significant evidence for case-control association combined with no or moderate evidence for ASP linkage can define a lower bound for the plausible RAFC . Using data from large type 2 diabetes (T2D) linkage and genome-wide association study meta-analyses, we find that under reasonable model assumptions, 23 of 36 autosomal T2D risk loci are unlikely to be due to causal variants with combined RAFC < 0.005, and four of the 23 are unlikely to be due to causal variants with combined RAFC < 0.05.
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Registered trials
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