Evidence map›Paper›PMID 31195969›Full record

Trial reportMolecular medicine (Cambridge, Mass.)2019

IgG Galactosylation status combined with MYOM2-rs2294066 precisely predicts anti-TNF response in ankylosing spondylitis.

Jing Liu, Qi Zhu, Jing Han, Hui Zhang, Yuan Li, Yanyun Ma, Dongyi He, Jianxin Gu, Xiaodong Zhou, John D Reveille and 4 more

Abstract readClinical Trial
In one paragraph

Trial report in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Machine Learning in Rheumatic Diseases.Clinical reviews in allergy & immunology · 2021
    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

14 authors.

Jing LiuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Qi ZhuInstitute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, Guanghua Integrative Medicine Hospital, Shanghai, China.
Jing HanDepartment of Biochemistry and Molecular Biology, Key Laboratory of Glycoconjugate Research Ministry of Public Health, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Hui ZhangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Yuan LiState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Yanyun MaMinistry of Education Key Laboratory of Contemporary Anthropology, Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University, Shanghai, China.
Dongyi HeInstitute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, Guanghua Integrative Medicine Hospital, Shanghai, China.
Jianxin GuDepartment of Biochemistry and Molecular Biology, Key Laboratory of Glycoconjugate Research Ministry of Public Health, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Xiaodong ZhouDivision of Rheumatology and Clinical Immunogenetics, the University of Texas-McGovern Medical School, Houston, TX, USA.
John D ReveilleDivision of Rheumatology and Clinical Immunogenetics, the University of Texas-McGovern Medical School, Houston, TX, USA.
Li JinState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Hejian ZouDivision of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China. hjzou@fudan.edu.cn.
Shifang RenDepartment of Biochemistry and Molecular Biology, Key Laboratory of Glycoconjugate Research Ministry of Public Health, School of Basic Medical Sciences, Fudan University, Shanghai, China. renshifang@fudan.edu.cn.
Jiucun WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China. jcwang@fudan.edu.cn.

Funding

Studies of HLA Region Genomics in Systemic Sclerosis and Ankylosing SpondyilitisU01AI090909 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN, REVEILLE, JOHN DUFFIN · 2010 to 2014
$2.9M
NIAID NIH HHS U01 AI090909
6 · The paper itself

Abstract

backgroundTumor necrosis factor (TNF) blockers have a high efficacy in treating Ankylosing Spondylitis (AS), yet up to 40% of AS patients show poor or even no response to this treatment. In this paper, we aim to build an approach to predict the response prior to clinical treatment.

methodsAS patients during the active progression were included and treated with TNF blocker for 3 months. Patients who do not fulfill ASASAS40 were considered as poor responders. The Immunoglobulin G galactosylation (IgG-Gal) ratio representing the quantity of IgG galactosylation was calculated and candidate single nucleotide polymorphisms (SNPs) in patients treated with etanercept was obtained. Machine-learning models and cross-validation were conducted to predict responsiveness.

resultsBoth IgG-Gal ratio at each time point and differential IgG-Gal ratios between week 0 and weeks 2, 4, 8, 12 showed significant difference between responders and poor-responders. Area under curve (AUC) of the IgG-Gal ratio prediction model was 0.8 after cross-validation, significantly higher than current clinical indexes (C-reactive protein (CRP) = 0.65, erythrocyte sedimentation rate (ESR) = 0.59). The SNP MYOM2-rs2294066 was found to be significantly associated with responsiveness of etanercept treatment. A three-stage approach consisting of baseline IgG-Gal ratio, differential IgG-Gal ratio in 2 weeks, and rs2294066 genotype demonstrated the ability to precisely predict the response of anti-TNF therapy (100% for poor-responders, 98% for responders).

conclusionsCombination of different omics can more precisely to predict the response of TNF blocker and it is potential to be applied clinically in the future.

Indexed as

AdultAntirheumatic AgentsBlood SedimentationConnectinEtanerceptFemaleGenotypeGlycoproteinsGlycosylationHumansImmunoglobulin GMaleMiddle AgedPolymorphism, Single NucleotideSpondylitis, AnkylosingTumor Necrosis Factor-alphaAntirheumatic AgentsConnectinEtanerceptGlycoproteinsglycosylated IgGImmunoglobulin GMYOM2 protein, humanTumor Necrosis Factor-alphaAnkylosing spondylitisDrug response predictionIgG-gal ratioMYOM2-rs2294066TNF blocker

Identifiers

PMID31195969
PMCPMC6567531

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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.