Evidence map›Paper›PMID 25455875›Full record

Trial reportFertility and sterility2015

Follow-up to genome-wide linkage and admixture mapping studies implicates components of the extracellular matrix in susceptibility to and size of uterine fibroids.

Brahim Aissani, Kui Zhang, Howard Wiener

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Fertility and sterility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. AFrontiers in genetics · 2019
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  16. Genetic determinants of uterine fibroid size in the multiethnic NIEHS uterine fibroid study.International journal of molecular epidemiology and genetics · 2015
    Article
  17. 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

3 authors at 1 institution in 1 country.

Brahim AissaniDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama. Electronic address: baissani@uab.edu.
Kui ZhangDepartment of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama.
Howard WienerDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama.
University of Alabama at Birmingham · US

Funding

Genetic Determinants of Uterine Fibroids in African-American and Caucasian WomenR01HD064398 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AISSANI, BRAHIM · 2010 to 2013
$1.0M
NICHD NIH HHS R01 HD064398NICHD NIH HHS R01-HD064398
6 · The paper itself

Abstract

objectiveTo conduct a follow-up association mapping to independent genome-wide linkage and admixture mapping studies of uterine leiomyoma.

designCase-control, cross-sectional study.

settingNot applicable. PATIENT(S): A total of 1,045 premenopausal North American participants in the National Institute of Environmental Health Sciences Uterine Fibroid Study. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): We genotyped 2,772 single-nucleotide polymorphisms from candidate genes located in peaks of linkage (2q37, 3p21, 5p13, 10p11, 11p15, 12q14, and 17q25) or admixture linkage disequilibrium (2q37, 4p16.1, and 10q26) mapping and reported to have regulated expression in uterine fibroids. RESULT(S): We report significant associations of variant members of the collagen gene family with risk and tumor size, including missense variants in COL6A3 and COL13A, with replications in African American and European American study groups. Furthermore, the cell-matrix Rho GTPase-encoding ARHGAP26 gene, and MAN1C1, a gene encoding a Golgi mannosidase involved in the maturation of procollagens, emerged as new candidate uterine leiomyoma genes affecting both risk and tumor size. CONCLUSION(S): Our data converge onto a possible model of uterine leiomyoma pathogenesis resulting from altered regulation, maintenance, and/or renewal of the extracellular matrix.

Indexed as

AdultChromosome MappingExtracellular MatrixFemaleFollow-Up StudiesGenetic LinkageGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLeiomyomaMiddle AgedUterine Neoplasmscollagenextracellular matrixfibroidsNIEHS cohortPolymorphismsusceptibility

Identifiers

PMID25455875
PMCPMC4314358
OpenAlexW1986396337

What Socratic holds

Textmetadata
LicenceTDM
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.