Evidence map›Paper›PMID 31145635›Full record

ArticleAmerican journal of respiratory cell and molecular biology2019

The Oncogene ECT2 Contributes to a Hyperplastic, Proliferative Lung Epithelial Cell Phenotype in Idiopathic Pulmonary Fibrosis.

Henrik M Ulke, Kathrin Mutze, Mareike Lehmann, Darcy E Wagner, Katharina Heinzelmann, Andreas Günther, Oliver Eickelberg, Melanie Königshoff

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. Review
  9. Article
  10. Article
  11. Review
  12. Update in Interstitial Lung Disease 2019.American journal of respiratory and critical care medicine · 2020
    Review
  13. Article
  14. Idiopathic Pulmonary Fibrosis and Lung Cancer: Finding Similarities within Differences.American journal of respiratory cell and molecular biology · 2019
    Article
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Henrik M UlkeLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.
Kathrin MutzeLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.
Mareike LehmannLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.
Darcy E WagnerLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.ORCID 0000-0003-3794-1309
Katharina HeinzelmannLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.ORCID 0000-0002-6904-4904
Andreas GüntherDepartment of Internal Medicine, Universities of Giessen and Marburg Lung Center, Justus Liebig University Giessen, Member of the German Center for Lung Research, Giessen, Germany; and.
Oliver EickelbergDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado, Denver, Aurora, Colorado.ORCID 0000-0001-7170-0360
Melanie KönigshoffLung Repair and Regeneration, Comprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Großhadern, and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany.
Helmholtz Zentrum München · DEJustus-Liebig-Universität Gießen · DELund University · SEUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) and lung cancer are progressive lung diseases with a poor prognosis. IPF is a risk factor for the development of lung cancer, and the incidence of lung cancer is increased in patients with IPF. The disease pathogenesis of IPF and lung cancer involves common genetic alterations, dysregulated pathways, and the emergence of hyperplastic and metaplastic epithelial cells. Here, we aimed to identify novel, common mediators that might contribute to epithelial cell reprogramming in IPF. Gene set enrichment analysis of publicly available non-small cell lung cancer and IPF datasets revealed a common pattern of misregulated genes linked to cell proliferation and transformation. The oncogene

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell ProliferationEpithelial CellsHumansHyperplasiaIdiopathic Pulmonary FibrosisLungLung NeoplasmsMicePhenotypeProto-Oncogene ProteinsECT2 protein, humanEct2 protein, mouseProto-Oncogene Proteinsalveolar epithelial cellsgene set enrichment analysislung cancerlung fibrosisoncogenic pathways

Identifiers

PMID31145635
OpenAlexW2946897582

What OpenQuestion 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 OpenQuestion graph.