Evidence map›Paper›PMID 31686270›Full record

ReviewCurrent diabetes reports2019

The Genetic Contribution to Type 1 Diabetes.

Marina Bakay, Rahul Pandey, Struan F A Grant, Hakon Hakonarson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. The role of mGenes & diseases · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Type 1Micromachines · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. The missing heritability in type 1 diabetes.Diabetes, obesity & metabolism · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Marina BakayThe Center for Applied Genomics, Division of Human Genetics, The Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Abramson Research Center, Suite 1216B, Philadelphia, PA, 19104-4318, USA.
Rahul PandeyThe Center for Applied Genomics, Division of Human Genetics, The Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Abramson Research Center, Suite 1216B, Philadelphia, PA, 19104-4318, USA.
Struan F A GrantThe Center for Applied Genomics, Division of Human Genetics, The Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Abramson Research Center, Suite 1216B, Philadelphia, PA, 19104-4318, USA.
Hakon HakonarsonThe Center for Applied Genomics, Division of Human Genetics, The Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Abramson Research Center, Suite 1216B, Philadelphia, PA, 19104-4318, USA. hakonarson@email.chop.edu.
Children's Hospital of Philadelphia · US

Funding

Genome Wide Association Study of Latent Autoimmune Diabetes in AdultsR01DK085212 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI GRANT, STRUAN F A · 2011 to 2016
$3.4M
NIDDK NIH HHS R01 DK085212
6 · The paper itself

Abstract

purpose of reviewTo provide an updated summary of discoveries made to date resulting from genome-wide association study (GWAS) and sequencing studies, and to discuss the latest loci added to the growing repertoire of genetic signals predisposing to type 1 diabetes (T1D). RECENT

findingsGenetic studies have identified over 60 loci associated with T1D susceptibility. GWAS alone does not specifically inform on underlying mechanisms, but in combination with other sequencing and omics-data, advances are being made in our understanding of T1D genetic etiology and pathogenesis. Current knowledge indicates that genetic variation operating in both pancreatic β cells and in immune cells is central in mediating T1D risk. One of the main challenges is to determine how these recently discovered GWAS-implicated variants affect the expression and function of gene products. Once we understand the mechanism of action for disease-causing variants, we will be well placed to apply targeted genomic approaches to impede the premature activation of the immune system in an effort to ultimately prevent the onset of T1D.

Indexed as

Diabetes Mellitus, Type 1Genome-Wide Association StudyInsulin-Secreting CellsGenetic Predisposition to DiseaseGenomicsHumansPolymorphism, Single NucleotideProspective StudiesAutoimmunityC-type lectin-like domain family 16A (CLEC16A) geneGenome-wide association study (GWAS)Susceptibility lociType 1 diabetes (T1D)

Identifiers

PMID31686270
OpenAlexW2982817576

What OpenQuestion holds

Textmetadata
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.