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Record W2983449145 · doi:10.1164/rccm.201905-1017oc

Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis

2019· article· en· W2983449145 on OpenAlexafffund
Richard J. Allen, Beatriz Guillén‐Guío, Justin M. Oldham, Shwu‐Fan Ma, Amy Dressen, Megan L. Paynton, Luke M. Kraven, Ma’en Obeidat, Xuan Li, Michael Ng, Rebecca Braybrooke, María Molina‐Molina, Brian D. Hobbs, Rachel K. Putman, Phuwanat Sakornsakolpat, Helen Booth, William A. Fahy, Simon P. Hart, Mike Hill, Nik Hirani, Richard Hubbard, Robin J. McAnulty, Ann Millar, Vidya Navaratnam, Eunice Oballa, Helen Parfrey, Gauri Saini, Moira K. B. Whyte, Yingze Zhang, Naftali Kaminski, Ayodeji Adegunsoye, Mary E. Strek, Margaret Neighbors, Xuting R. Sheng, Gunnar Guðmundsson, Vilmundur Guðnason, Hiroto Hatabu, David J. Lederer, Ani Manichaikul, John D. Newell, George O'connor, Victor E. Ortega, Hanfei Xu, Tasha E. Fingerlin, Yohan Bossé, Ke Hao, Philippe Joubert, David C. Nickle, Don D. Sin, Wim Timens, Dominic Furniss, Andrew P. Morris, Krina T. Zondervan, Ian P. Hall, Ian Sayers, Martin D. Tobin, Toby M. Maher, Michael H. Cho, Gary M. Hunninghake, David A. Schwartz, Brian L. Yaspan, Philip L. Molyneaux, Carlos Flores, Imre Noth, Gísli Jenkins, Louise V. Wain

Bibliographic record

VenueAmerican Journal of Respiratory and Critical Care Medicine · 2019
Typearticle
Languageen
FieldMedicine
TopicInterstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Canadian institutionsInstitut universitaire de cardiologie et de pneumologie de QuébecUniversité LavalSt. Paul's HospitalUniversity of British Columbia
FundersNIHR Nottingham Biomedical Research CentreAgencia Estatal de InvestigaciónNational Institute of Diabetes and Digestive and Kidney DiseasesInstituto de Salud Carlos IIIMedical Research CouncilNational Institutes of HealthUniversity of LeicesterAsthma and Lung UKNational Heart, Lung, and Blood InstituteBritish Lung FoundationNIHR Leicester Biomedical Research CentreMinisterio de Ciencia, Innovación y UniversidadesMichael Smith Health Research BCInstituto Tecnológico y de Energías RenovablesEuropean Regional Development FundEuropean CommissionBroad InstituteNational Center for Advancing Translational SciencesWellcome TrustNational Institute for Health and Care ResearchU.S. Department of Veterans Affairs
KeywordsIdiopathic pulmonary fibrosisGenome-wide association studyMedicineGenetic associationGenetic predispositionLung cancerGeneLungDiseaseGeneticsBiologySingle-nucleotide polymorphismPathologyGenotypeInternal medicine

Abstract

fetched live from OpenAlex

Abstract Rationale Idiopathic pulmonary fibrosis (IPF) is a complex lung disease characterized by scarring of the lung that is believed to result from an atypical response to injury of the epithelium. Genome-wide association studies have reported signals of association implicating multiple pathways including host defense, telomere maintenance, signaling, and cell–cell adhesion. Objectives To improve our understanding of factors that increase IPF susceptibility by identifying previously unreported genetic associations. Methods We conducted genome-wide analyses across three independent studies and meta-analyzed these results to generate the largest genome-wide association study of IPF to date (2,668 IPF cases and 8,591 controls). We performed replication in two independent studies (1,456 IPF cases and 11,874 controls) and functional analyses (including statistical fine-mapping, investigations into gene expression, and testing for enrichment of IPF susceptibility signals in regulatory regions) to determine putatively causal genes. Polygenic risk scores were used to assess the collective effect of variants not reported as associated with IPF. Measurements and Main Results We identified and replicated three new genome-wide significant (P < 5 × 10−8) signals of association with IPF susceptibility (associated with altered gene expression of KIF15, MAD1L1, and DEPTOR) and confirmed associations at 11 previously reported loci. Polygenic risk score analyses showed that the combined effect of many thousands of as yet unreported IPF susceptibility variants contribute to IPF susceptibility. Conclusions The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis. New signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.003
metaresearch head score (Gemma)0.006
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.005
Threshold uncertainty score0.013

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0030.006
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0010.002
Science and technology studies0.0010.001
Scholarly communication0.0010.000
Open science0.0010.001
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.012
GPT teacher head0.292
Teacher spread0.281 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations341
Published2019
Admission routes2
Has abstractyes

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