ArticleGenetic epidemiology2014
Methods for collapsing multiple rare variants in whole-genome sequence data.
Article in Genetic epidemiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Assessment of the functionality and usability of open-source rare variant analysis pipelines.Briefings in bioinformatics · 2025Pooled it
- Genetic Factors and Long-term Treatment-Related Neurocognitive Deficits, Anxiety, and Depression in Childhood Leukemia Survivors: An Exome-Wide Association Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024Article
- Genetic factors in treatment-related cardiovascular complications in survivors of childhood acute lymphoblastic leukemia.Pharmacogenomics · 2021Article
- Rare variant association testing in the non-coding genome.Human genetics · 2020Review
- Investigation of novel variations of ORAI1 gene and their association with Kawasaki disease.Journal of human genetics · 2019Article
- Article
- FastSKAT: Sequence kernel association tests for very large sets of markers.Genetic epidemiology · 2018Article
- Family-based tests for associating haplotypes with general phenotype data: Improving the FBAT-haplotype algorithm.Genetic epidemiology · 2018Article
- Longitudinal data analysis for rare variants detection with penalized quadratic inference function.Scientific reports · 2017Article
- The Increasing Importance of Gene-Based Analyses.PLoS genetics · 2016Review
- Summary of results and discussions from the gene-based tests group at Genetic Analysis Workshop 18.Genetic epidemiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Genetic Analysis Workshop 18 provided whole-genome sequence data in a pedigree-based sample and longitudinal phenotype data for hypertension and related traits, presenting an excellent opportunity for evaluating analysis choices. We summarize the nine contributions to the working group on collapsing methods, which evaluated various approaches for the analysis of multiple rare variants. One contributor defined a variant prioritization scheme, whereas the remaining eight contributors evaluated statistical methods for association analysis. Six contributors chose the gene as the genomic region for collapsing variants, whereas three contributors chose nonoverlapping sliding windows across the entire genome. Statistical methods spanned most of the published methods, including well-established burden tests, variance-components-type tests, and recently developed hybrid approaches. Lesser known methods, such as functional principal components analysis, higher criticism, and homozygosity association, and some newly introduced methods were also used. We found that performance of these methods depended on the characteristics of the genomic region, such as effect size and direction of variants under consideration. Except for MAP4 and FLT3, the performance of all statistical methods to identify rare casual variants was disappointingly poor, providing overall power almost identical to the type I error. This poor performance may have arisen from a combination of (1) small sample size, (2) small effects of most of the causal variants, explaining a small fraction of variance, (3) use of incomplete annotation information, and (4) linkage disequilibrium between causal variants in a gene and noncausal variants in nearby genes. Our findings demonstrate challenges in analyzing rare variants identified from sequence data.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.