Evidence map›Paper›PMID 33735170›Full record

ArticlePLoS computational biology2021

Boosting GWAS using biological networks: A study on susceptibility to familial breast cancer.

Héctor Climente-González, Christine Lonjou, Fabienne Lesueur, GENESIS study group, Dominique Stoppa-Lyonnet, Nadine Andrieu, Chloé-Agathe Azencott

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Update on the relationship between theThe Journal of international medical research · 2023
    Pooled it
  2. Article
  3. Review
  4. Article
  5. The electroneutral NaAmerican journal of physiology. Cell physiology · 2024
    Article
  6. Omics-Based Investigations of Breast Cancer.Molecules (Basel, Switzerland) · 2023
    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

7 authors at 2 institutions in 2 countries.

Héctor Climente-GonzálezInstitut Curie, PSL Research University, Paris, France.ORCID 0000-0002-3030-7471
Christine LonjouInstitut Curie, PSL Research University, Paris, France.ORCID 0000-0003-1226-6992
Fabienne LesueurInstitut Curie, PSL Research University, Paris, France.ORCID 0000-0001-7404-4549
GENESIS study group
Dominique Stoppa-LyonnetService de Génétique, Institut Curie, Paris, France.ORCID 0000-0002-5438-8309
Nadine AndrieuInstitut Curie, PSL Research University, Paris, France.
Chloé-Agathe AzencottInstitut Curie, PSL Research University, Paris, France.ORCID 0000-0003-1003-301X
Inserm · FRDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) explore the genetic causes of complex diseases. However, classical approaches ignore the biological context of the genetic variants and genes under study. To address this shortcoming, one can use biological networks, which model functional relationships, to search for functionally related susceptibility loci. Many such network methods exist, each arising from different mathematical frameworks, pre-processing steps, and assumptions about the network properties of the susceptibility mechanism. Unsurprisingly, this results in disparate solutions. To explore how to exploit these heterogeneous approaches, we selected six network methods and applied them to GENESIS, a nationwide French study on familial breast cancer. First, we verified that network methods recovered more interpretable results than a standard GWAS. We addressed the heterogeneity of their solutions by studying their overlap, computing what we called the consensus. The key gene in this consensus solution was COPS5, a gene related to multiple cancer hallmarks. Another issue we observed was that network methods were unstable, selecting very different genes on different subsamples of GENESIS. Therefore, we proposed a stable consensus solution formed by the 68 genes most consistently selected across multiple subsamples. This solution was also enriched in genes known to be associated with breast cancer susceptibility (BLM, CASP8, CASP10, DNAJC1, FGFR2, MRPS30, and SLC4A7, P-value = 3 × 10-4). The most connected gene was CUL3, a regulator of several genes linked to cancer progression. Lastly, we evaluated the biases of each method and the impact of their parameters on the outcome. In general, network methods preferred highly connected genes, even after random rewirings that stripped the connections of any biological meaning. In conclusion, we present the advantages of network-guided GWAS, characterize their shortcomings, and provide strategies to address them. To compute the consensus networks, implementations of all six methods are available at https://github.com/hclimente/gwas-tools.

Indexed as

Breast NeoplasmsAlgorithmsDatabases, GeneticFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPolymorphism, Single Nucleotide

Identifiers

PMID33735170
PMCPMC8009366
OpenAlexW3136093638

What Socratic 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 Socratic graph.