Evidence map›Paper›PMID 34659337›Full record

ReviewFrontiers in genetics2021

From GWAS to Gene: Transcriptome-Wide Association Studies and Other Methods to Functionally Understand GWAS Discoveries.

Binglan Li, Marylyn D Ritchie

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 3 pooled it
17.0field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 3 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Unveiling novel susceptibility genes for sarcoidosis by a cross-tissue transcriptome-wide association study.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

42 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 at 2 institutions in 1 country.

Binglan LiDepartment of Biomedical Data Science, Stanford University, Stanford, CA, United States.
Marylyn D RitchieDepartment of Genetics, University of Pennsylvania, Philadelphia, PA, United States.
Stanford University · USUniversity of Pennsylvania · US

Funding

Pharmacogenomics of HIV TherapyR01AI077505 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HAAS, DAVID W · 2008 to 2025
$12.3M
NIAID NIH HHS R01 AI077505
6 · The paper itself

Abstract

Since their inception, genome-wide association studies (GWAS) have identified more than a hundred thousand single nucleotide polymorphism (SNP) loci that are associated with various complex human diseases or traits. The majority of GWAS discoveries are located in non-coding regions of the human genome and have unknown functions. The valley between non-coding GWAS discoveries and downstream affected genes hinders the investigation of complex disease mechanism and the utilization of human genetics for the improvement of clinical care. Meanwhile, advances in high-throughput sequencing technologies reveal important genomic regulatory roles that non-coding regions play in the transcriptional activities of genes. In this review, we focus on data integrative bioinformatics methods that combine GWAS with functional genomics knowledge to identify genetically regulated genes. We categorize and describe two types of data integrative methods. First, we describe fine-mapping methods. Fine-mapping is an exploratory approach that calibrates likely causal variants underneath GWAS signals. Fine-mapping methods connect GWAS signals to potentially causal genes through statistical methods and/or functional annotations. Second, we discuss gene-prioritization methods. These are hypothesis generating approaches that evaluate whether genetic variants regulate genes via certain genetic regulatory mechanisms to influence complex traits, including colocalization, mendelian randomization, and the transcriptome-wide association study (TWAS). TWAS is a gene-based association approach that investigates associations between genetically regulated gene expression and complex diseases or traits. TWAS has gained popularity over the years due to its ability to reduce multiple testing burden in comparison to other variant-based analytic approaches. Multiple types of TWAS methods have been developed with varied methodological designs and biological hypotheses over the past 5 years. We dive into discussions of how TWAS methods differ in many aspects and the challenges that different TWAS methods face. Overall, TWAS is a powerful tool for identifying complex trait-associated genes. With the advent of single-cell sequencing, chromosome conformation capture, gene editing technologies, and multiplexing reporter assays, we are expecting a more comprehensive understanding of genomic regulation and genetically regulated genes underlying complex human diseases and traits in the future.

Indexed as

data integrationeQTLfine-mappingfunctional annotationGWASsummary statisticsTWAS

Identifiers

PMID34659337
PMCPMC8515949
OpenAlexW3203277023

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.