Evidence map›Paper›PMID 27490795›Full record

ArticlePloS one2016

Six-SOMAmer Index Relating to Immune, Protease and Angiogenic Functions Predicts Progression in IPF.

Shanna L Ashley, Meng Xia, Susan Murray, David N O'Dwyer, Ethan Grant, Eric S White, Kevin R Flaherty, Fernando J Martinez, Bethany B Moore

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
6.4field-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, 63 citations in OpenAlex.

  1. Prognosis of idiopathic pulmonary fibrosis without anti-fibrotic therapy: a systematic review.European respiratory review : an official journal of the European Respiratory Society · 2020
    Pooled it
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  10. The Role of Ficolins in Lung Injury.Journal of innate immunity · 2024
    Review
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  12. Article
  13. The Mammalian Cysteine Protease Legumain in Health and Disease.International journal of molecular sciences · 2022
    Review
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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

9 authors at 2 institutions in 1 country.

Shanna L AshleyGraduate Program in Immunology, University of Michigan, Ann Arbor, MI, United States of America.
Meng XiaBiostatistics Department, University of Michigan School of Public Health, Ann Arbor, MI, United States of America.
Susan MurrayBiostatistics Department, University of Michigan School of Public Health, Ann Arbor, MI, United States of America.
David N O'DwyerPulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States of America.
Ethan GrantMedImmune, Gaithersburg, MD, United States of America.
Eric S WhitePulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States of America.
Kevin R FlahertyPulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States of America.
Fernando J MartinezDepartment of Internal Medicine, Weill Cornell Medical College, New York, NY, United States of America.
Bethany B MoorePulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States of America.ORCID http://orcid.org/0000-0003-3051-745X
University of Michigan · USCornell University · US

Funding

Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Periostin Regulation of Lung FibrosisR01HL115618 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2013 to 2016
$1.6M
NCATS NIH HHS UL1 TR000433NHLBI NIH HHS R01 HL115618NIAID NIH HHS T32 AI007413
6 · The paper itself

Abstract

rationaleBiomarkers in easily accessible compartments like peripheral blood that can predict disease progression in idiopathic pulmonary fibrosis (IPF) would be clinically useful regarding clinical trial participation or treatment decisions for patients. In this study, we used unbiased proteomics to identify relevant disease progression biomarkers in IPF.

methodsPlasma from IPF patients was measured using an 1129 analyte slow off-rate modified aptamer (SOMAmer) array, and patient outcomes were followed over the next 80 weeks. Receiver operating characteristic (ROC) curves evaluated sensitivity and specificity for levels of each biomarker and estimated area under the curve (AUC) when prognostic biomarker thresholds were used to predict disease progression. Both logistic and Cox regression models advised biomarker selection for a composite disease progression index; index biomarkers were weighted via expected progression-free days lost during follow-up with a biomarker on the unfavorable side of the threshold.

resultsA six-analyte index, scaled 0 to 11, composed of markers of immune function, proteolysis and angiogenesis [high levels of ficolin-2 (FCN2), cathepsin-S (Cath-S), legumain (LGMN) and soluble vascular endothelial growth factor receptor 2 (VEGFsR2), but low levels of inducible T cell costimulator (ICOS) or trypsin 3 (TRY3)] predicted better progression-free survival in IPF with a ROC AUC of 0.91. An index score ≥ 3 (group ≥ 2) was strongly associated with IPF progression after adjustment for age, gender, smoking status, immunomodulation, forced vital capacity % predicted and diffusing capacity for carbon monoxide % predicted (HR 16.8, 95% CI 2.2-126.7, P = 0.006).

conclusionThis index, derived from the largest proteomic analysis of IPF plasma samples to date, could be useful for clinical decision making in IPF, and the identified analytes suggest biological processes that may promote disease progression.

Indexed as

Severity of Illness IndexAgedArea Under CurveAsparaginyl EndopeptidaseBiomarkersCathepsinsCysteine EndopeptidasesDisease-Free SurvivalDisease ProgressionFemaleFicolinsHumansIdiopathic Pulmonary FibrosisInducible T-Cell Co-Stimulator ProteinLectinsLogistic ModelsAsparaginyl EndopeptidaseBiomarkersCathepsinsCysteine EndopeptidasesFicolinsInducible T-Cell Co-Stimulator ProteinKDR protein, humanLectinsPeptide HydrolasesVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID27490795
PMCPMC4973878
OpenAlexW2475562838

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.