Evidence map›Paper›PMID 27313329›Full record

ArticleBlood2016

Genetic risk factors for sclerotic graft-versus-host disease.

Yoshihiro Inamoto, Paul J Martin, Mary E D Flowers, Stephanie J Lee, Paul A Carpenter, Edus H Warren, Daniel E Geraghty, Ni Lee, Michael J Boeckh, Barry E Storer and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.

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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 2 institutions in 1 country.

Yoshihiro InamotoDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA;
Paul J MartinDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Medicine, and.ORCID 0000-0001-9051-1215
Mary E D FlowersDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Medicine, and.
Stephanie J LeeDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Medicine, and.
Paul A CarpenterDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Pediatrics, University of Washington School of Medicine, Seattle, WA;
Edus H WarrenDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Medicine, and.
Daniel E GeraghtyDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA;
Ni LeeDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA;
Michael J BoeckhDepartment of Medicine, and Division of Vaccine and Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, WA;
Barry E StorerDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA;
David M LevineDepartment of Biostatics, University of Washington School of Medicine, Seattle, WA; and.
Wenhong FanDivision of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA.
Lue-Ping ZhaoDepartment of Biostatics, University of Washington School of Medicine, Seattle, WA; and Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA.
John A HansenDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Medicine, and.
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

VIRUS-MEDIATED MYELOSUPPRESSIONP01CA018029 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Geoffrey Roger HILL · 1985 to 2026
$128.4M
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) OutcomeR01HL105914 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MARTIN, PAUL J · 2011 to 2019
$9.8M
Improving Outcomes Assessment in Chronic GVHDR01CA118953 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LEE, STEPHANIE J · 2011 to 2025
$8.3M
Whole Genome Association Analysis of Hematopoietic Cell Transplant OutcomeR01HL087690 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HANSEN, JOHN ANDREW · 2006 to 2008
$4.1M
Infections in Hematopoietic Cell Transplant RecipientsK24HL093294 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BOECKH, MICHAEL J · 2009 to 2019
$1.5M
NCI NIH HHS P01 CA018029NCI NIH HHS R01 CA118953NHLBI NIH HHS K24 HL093294NHLBI NIH HHS R01 HL087690NHLBI NIH HHS R01 HL105914
6 · The paper itself

Abstract

Sclerotic graft-versus-host disease (GVHD) is a distinctive phenotype of chronic GVHD after allogeneic hematopoietic cell transplantation, characterized by fibrosis of skin or fascia. Sclerotic GVHD has clinical and histopathological similarities with systemic sclerosis, an autoimmune disease whose risk is influenced by genetic polymorphisms. We examined 13 candidate single-nucleotide polymorphisms (SNPs) that have a well-documented association with systemic sclerosis to determine whether these SNPs are also associated with the risk of sclerotic GVHD. The study cohort included 847 consecutive patients who were diagnosed with chronic GVHD. Genotyping was performed using microarrays, followed by imputation of unobserved SNPs. The donor rs10516487 (BANK1: B-cell scaffold protein with ankyrin repeats 1) TT genotype was associated with lower risk of sclerotic GVHD (hazard ratio [HR], 0.43; 95% confidence interval [CI], 0.21-0.87; P = .02). Donor and recipient rs2056626 (CD247: T-cell receptor ζ subunit) GG or GT genotypes were associated with higher risk of sclerotic GVHD (HR, 1.57; 95% CI, 1.13-2.18; P = .007 and HR, 1.66; 95% CI, 1.19-2.32; P = .003, respectively). Donor and recipient rs987870 (5'-flanking region of HLA-DPA1) CC genotypes were associated with higher risk of sclerotic GVHD (HR, 2.50; 95% CI, 1.22-5.11; P = .01 and HR, 2.13; 95% CI, 1.00-4.54; P = .05, respectively). In further analyses, the recipient DPA1*01:03∼DPB1*04:01 haplotype and certain amino acid substitutions in the recipient P1 peptide-binding pocket of the HLA-DP heterodimer were associated with risk of sclerotic GVHD. Genetic components associated with systemic sclerosis are also associated with sclerotic GVHD. HLA-DP-mediated antigen presentation, T-cell response, and B-cell activation have important roles in the pathogenic mechanisms of both diseases.

Indexed as

Adaptor Proteins, Signal TransducingAdolescentAdultAgedAntigens, CDAntigens, NeoplasmB-LymphocytesChildChild, PreschoolCohort StudiesFemaleFollow-Up StudiesGenotypeGraft vs Host DiseaseHaplotypesHematopoietic Stem Cell TransplantationAdaptor Proteins, Signal TransducingAntigens, CDAntigens, NeoplasmBANK1 protein, humanCD248 protein, humanHLA-DPA1 antigenHLA-DP alpha-ChainsMembrane Proteins

Identifiers

PMID27313329
PMCPMC5025901
OpenAlexW2429621985

What Socratic 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 Socratic graph.