Evidence map›Paper›PMID 26789141›Full record

ArticleAmerican journal of medical genetics. Part A2016

Evaluation of proton-coupled folate transporter (SLC46A1) polymorphisms as risk factors for neural tube defects and oral clefts.

Julia E VanderMeer, Tonia C Carter, Faith Pangilinan, Adam Mitchell, Emma Kurnat-Thoma, Peadar N Kirke, James F Troendle, Anne M Molloy, Ronald G Munger, Marcia L Feldkamp and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of medical genetics. Part A, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Mutations in folate transporter genes and risk for human myelomeningocele.American journal of medical genetics. Part A · 2017
    Article
  4. Article
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

14 authors at 8 institutions in 2 countries.

Julia E VanderMeerSection of Molecular Pathogenesis, Medical Genomics Metabolic Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland.
Tonia C CarterDivision of Intramural Population Health Research, Department of Health and Human Services, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland.
Faith PangilinanSection of Molecular Pathogenesis, Medical Genomics Metabolic Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland.
Adam MitchellSection of Molecular Pathogenesis, Medical Genomics Metabolic Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland.
Emma Kurnat-ThomaSection of Molecular Pathogenesis, Medical Genomics Metabolic Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland.
Peadar N KirkeUnit of Child Health Epidemiology, Health Research Board, Dublin, Ireland.
James F TroendleOffice of Biostatistics Research, Department of Health and Human Services, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland.
Anne M MolloyDepartment of Clinical Medicine, Trinity College Dublin, Dublin, Ireland.
Ronald G MungerDepartment of Nutrition, Dietetics and Food Sciences, Utah State University, Logan, Utah.
Marcia L FeldkampDivision of Medical Genetics, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Maria A MansillaDivision of Neonatology, Department of Pediatrics, University of Iowa, Iowa City, Iowa.
James L MillsDivision of Intramural Population Health Research, Department of Health and Human Services, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland.
Jeff C MurrayDivision of Neonatology, Department of Pediatrics, University of Iowa, Iowa City, Iowa.
Lawrence C BrodySection of Molecular Pathogenesis, Medical Genomics Metabolic Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland.
National Human Genome Research Institute · USNational Institutes of Health · USUniversity of Iowa · USHealth Research Board · IENational Heart Lung and Blood Institute · USTrinity College Dublin · IEUniversity of Utah · USUtah State University · US

Funding

The contribution folate and vitamin B12 genes to disease.ZIAHG000167 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BRODY, LAWRENCE C · 2009 to 2025
$17.6M
NICHD Health Research Board Of Ireland Neural Tube Defects StudyZIAHD002502 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MILLS, JAMES · 2009 to 2022
$2.9M
NICHD-HEALTH RESEARCH BROAD OF IRELAND NEURAL TUBE DEFECTS STUDYZ01HD002502 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MILLS, JAMES L · 1993 to 2008
$1.2M
Intramural NIH HHS Z01 HD002502
6 · The paper itself

Abstract

Many folate-related genes have been investigated for possible causal roles in neural tube defects (NTDs) and oral clefts. However, no previous reports have examined the major gene responsible for folate uptake, the proton-coupled folate transporter (SLC46A1). We tested for association between these birth defects and single nucleotide polymorphisms in the SLC46A1 gene. The NTD study population included 549 complete and incomplete case-family triads, and 999 controls from Ireland. The oral clefts study population comprised a sample from Utah (495 complete and incomplete case-family triads and 551 controls) and 221 Filipino multiplex cleft families. There was suggestive evidence of increased NTD case risk with the rs17719944 minor allele (odds ratio (OR): 1.29; 95% confidence intervals (CI): [1.00-1.67]), and decreased maternal risk of an NTD pregnancy with the rs4795436 minor allele (OR: 0.62; [0.39-0.99]). In the Utah sample, the rs739439 minor allele was associated with decreased case risk for cleft lip with cleft palate (genotype relative risk (GRR): 0.56 [0.32-0.98]). Additionally, the rs2239907 minor allele was associated with decreased case risk for cleft lip with cleft palate in several models, and with cleft palate only in a recessive model (OR: 0.41; [0.20-0.85]). These associations did not remain statistically significant after correcting for multiple hypothesis testing. Nominal associations between SLC46A1 polymorphisms and both Irish NTDs and oral clefts in the Utah population suggest some role in the etiology of these birth defects, but further investigation in other populations is needed.

Indexed as

Polymorphism, Single NucleotideAllelesCase-Control StudiesCleft LipGene FrequencyGenetic Association StudiesGenotypeHumansNeural Tube DefectsProton-Coupled Folate TransporterRisk FactorsProton-Coupled Folate TransporterSLC46A1 protein, humancleft lipcleft palatefolatefolate transportfolic acidneural tubeoral cleftsproton-coupled folate transporter

Identifiers

PMID26789141
PMCPMC6205290
OpenAlexW2255217257

What OpenQuestion holds

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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.