Evidence map›Paper›PMID 26921334›Full record

ArticleCancer research2016

Extracellular Adenosine Production by ecto-5'-Nucleotidase (CD73) Enhances Radiation-Induced Lung Fibrosis.

Florian Wirsdörfer, Simone de Leve, Federica Cappuccini, Therese Eldh, Alina V Meyer, Eva Gau, Linda F Thompson, Ning-Yuan Chen, Harry Karmouty-Quintana, Ute Fischer and 7 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.5field-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

51 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
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  9. Review
  10. Review
  11. The Clinical Significance of CD73 in Cancer.International journal of molecular sciences · 2023
    Review
  12. Article
  13. ENPP1 Immunobiology as a Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Review
  14. Article
  15. CD73: Friend or Foe in Lung Injury.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Article
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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

17 authors at 8 institutions in 2 countries.

Florian WirsdörferInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Simone de LeveInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Federica CappucciniInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Therese EldhDepartment of Radiation Oncology, University Hospital Tübingen, Tübingen, Germany.
Alina V MeyerInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Eva GauInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Linda F ThompsonImmunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma.
Ning-Yuan ChenDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, Texas.
Harry Karmouty-QuintanaDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, Texas.
Ute FischerDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Clinic, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Michael KasperInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
Diana KleinInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
Jerry W RitcheyDepartment of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, Oklahoma.
Michael R BlackburnDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, Texas.
Astrid M WestendorfDepartment of Infection Immunology, Institute of Medical Microbiology, Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Martin StuschkeDepartment of Radiation Oncology, University Hospital Essen, Essen, Germany.
Verena JendrossekInstitute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany. verena.jendrossek@uni-due.de.
University of Duisburg-Essen · DEThe University of Texas Health Science Center at Houston · USEssen University Hospital · DEHeinrich Heine University Düsseldorf · DEOklahoma Medical Research Foundation · USOklahoma State University · USUniversity Children's Hospital Tübingen · DEUniversity Hospital Carl Gustav Carus · DE

Funding

Trangenic Mouse Breeding CoreP01HL114457 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 2013 to 2017
$10.0M
The Regulation of Inflammatory Responses by CD73R01AI018220 · NIAID · SCRIPPS CLINIC AND RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 1985 to 2012
$3.1M
NHLBI NIH HHS P01 HL114457NIAID NIH HHS R01 AI018220
6 · The paper itself

Abstract

Radiation-induced pulmonary fibrosis is a severe side effect of thoracic irradiation, but its pathogenesis remains poorly understood and no effective treatment is available. In this study, we investigated the role of the extracellular adenosine as generated by the ecto-5'-nucleotidase CD73 in fibrosis development after thoracic irradiation. Exposure of wild-type C57BL/6 mice to a single dose (15 Gray) of whole thorax irradiation triggered a progressive increase in CD73 activity in the lung between 3 and 30 weeks postirradiation. In parallel, adenosine levels in bronchoalveolar lavage fluid (BALF) were increased by approximately 3-fold. Histologic evidence of lung fibrosis was observed by 25 weeks after irradiation. Conversely, CD73-deficient mice failed to accumulate adenosine in BALF and exhibited significantly less radiation-induced lung fibrosis (P < 0.010). Furthermore, treatment of wild-type mice with pegylated adenosine deaminase or CD73 antibodies also significantly reduced radiation-induced lung fibrosis. Taken together, our findings demonstrate that CD73 potentiates radiation-induced lung fibrosis, suggesting that existing pharmacologic strategies for modulating adenosine may be effective in limiting lung toxicities associated with the treatment of thoracic malignancies. Cancer Res; 76(10); 3045-56. ©2016 AACR.

Indexed as

Disease Models, AnimalRadiation, Ionizing5'-NucleotidaseAdenosineAnimalsApoptosisBlotting, WesternCell ProliferationGPI-Linked ProteinsHumansImmunoenzyme TechniquesMiceMice, Inbred C57BLMice, KnockoutPulmonary FibrosisReal-Time Polymerase Chain Reaction5'-NucleotidaseAdenosineGPI-Linked ProteinsNt5e protein, mouseRNA, Messenger

Identifiers

PMID26921334
PMCPMC4960984
OpenAlexW2285222319

What OpenQuestion holds

Textmetadata
LicenceTDM
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.