Evidence map›Paper›PMID 22128050›Full record

ArticleGenetic epidemiology2011

Lessons learned from Genetic Analysis Workshop 17: transitioning from genome-wide association studies to whole-genome statistical genetic analysis.

Alexander F Wilson, Andreas Ziegler

Abstract read
In one paragraph

Article in Genetic epidemiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. NIA Long Life Family Study: Objectives, Design, and Heritability of Cross-Sectional and Longitudinal Phenotypes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Article
  2. Review
  3. Article
  4. Article
  5. Cognitive, Linguistic, and Motor Abilities in a Multigenerational Family with Childhood Apraxia of Speech.Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists · 2016
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Alexander F WilsonGenometrics Section, Inherited Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, MD 21224, USA. afw@mail.nih.gov
Andreas Ziegler
National Institutes of Health · USUniversity Hospital Schleswig-Holstein · DE

Funding

Genometric analysis of quantitative traitsZIAHG000200 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI WILSON, ALEXANDER F · 2009 to 2020
$19.8M
GENETIC ANALYSIS OF COMMON DISEASES: AN EVALUATIONR01GM031575 · NIGMS · UNIVERSITY OF TEXAS RIO GRANDE VALLEY · PI ALMASY, LAURA A. · 1985 to 2016
$7.8M
Intramural NIH HHS Z99 HG999999Intramural NIH HHS Z99 HL999999Intramural NIH HHS Z99 MH999999Intramural NIH HHS ZIA HG000200NIGMS NIH HHS R01 GM031575
6 · The paper itself

Abstract

Genetic Analysis Workshop 17 (GAW17) focused on the transition from genome-wide association study designs and methods to the study designs and statistical genetic methods that will be required for the analysis of next-generation sequence data including both common and rare sequence variants. In the 166 contributions to GAW17, a wide variety of statistical methods were applied to simulated traits in population- and family-based samples, and results from these analyses were compared to the known generating model. In general, many of the statistical genetic methods used in the population-based sample identified causal sequence variants (SVs) when the estimated locus-specific heritability, as measured in the population-based sample, was greater than about 0.08. However, SVs with locus-specific heritabilities less than 0.03 were rarely identified consistently. In the family-based samples, many of the methods detected SVs that were rarer than those detected in the population-based sample, but the estimated locus-specific heritabilities for these rare SVs, as measured in the family-based samples, were substantially higher (>0.2) than their corresponding heritabilities in the population-based samples. Substantial inflation of the type I error rate was observed across a wide variety of statistical methods. Although many of the contributions found little inflation in type I error for Q4, a trait with no causal SVs, type I error rates for Q1 and Q2 were well above their nominal levels with the inflation for Q1 being higher than that for Q2. It seems likely that this inflation in type I error is due to correlations among SVs.

Indexed as

Models, GeneticModels, StatisticalCausalityGenetic Predisposition to DiseaseGenome-Wide Association StudyHuman Genome ProjectHumansMolecular EpidemiologyPolymorphism, Single NucleotideSensitivity and SpecificitySequence Analysis

Identifiers

PMID22128050
PMCPMC3277851
OpenAlexW2146182855

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 Socratic graph.