Evidence map›Paper›PMID 26157023›Full record

ReviewHuman molecular genetics2015

Strategies for fine-mapping complex traits.

Sarah L Spain, Jeffrey C Barrett

Abstract readReview
In one paragraph

Review in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

128 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Review
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  7. Article
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  12. fSuSiE enables fine-mapping of QTLs from genome-scale molecular profiles.bioRxiv : the preprint server for biology · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Review
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  18. Article
  19. Multivariate Bayesian variable selection for multi-trait genetic fine mapping.Journal of the Royal Statistical Society. Series C, Applied statistics · 2025
    Article
  20. Review

68 more citing papers are in PubMed but not listed here.

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.

Sarah L SpainWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1HH, UK.
Jeffrey C BarrettWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1HH, UK jb26@sanger.ac.uk.

Funding

Wellcome Trust WT098051
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have identified thousands of robust and replicable genetic associations for complex disease. However, the identification of the causal variants that underlie these associations has been more difficult. This problem of fine-mapping association signals predates GWAS, but the last few years have seen a surge of studies aimed at pinpointing causal variants using both statistical evidence from large association data sets and functional annotations of genetic variants. Combining these two approaches can often determine not only the causal variant but also the target gene. Recent contributions include analyses of custom genotyping arrays, such as the Immunochip, statistical methods to identify credible sets of causal variants and the addition of functional genomic annotations for coding and non-coding variation to help prioritize variants and discern functional consequence and hence the biological basis of disease risk.

Indexed as

Chromosome MappingAnimalsGenetic VariationGenome-Wide Association StudyGenotypeHumansPhenotype

Identifiers

PMID26157023
PMCPMC4572002

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.