Evidence map›Paper›PMID 32039023›Full record

ArticleFrontiers in oncology2019

The Multi-Modal Effect of the Anti-fibrotic Drug Pirfenidone on NSCLC.

Sebastian Marwitz, Kati Turkowski, Dörte Nitschkowski, Andreas Weigert, Julius Brandenburg, Norbert Reiling, Michael Thomas, Martin Reck, Daniel Drömann, Werner Seeger and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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

13 authors at 6 institutions in 1 country.

Sebastian MarwitzPathology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Kati TurkowskiMolecular Mechanisms in Lung Cancer, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Dörte NitschkowskiPathology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Andreas WeigertFaculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Julius BrandenburgMicrobial Interface Biology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Norbert ReilingMicrobial Interface Biology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Michael ThomasDepartment of Thoracic Oncology, University Hospital Heidelberg, Heidelberg, Germany.
Martin ReckAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Daniel DrömannAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Werner SeegerMolecular Mechanisms in Lung Cancer, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Klaus F RabeAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Rajkumar SavaiMolecular Mechanisms in Lung Cancer, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Torsten GoldmannPathology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Research Center Borstel - Leibniz Lung Center · DEGerman Center for Lung Research · DEJustus-Liebig-Universität Gießen · DELungenClinic Grosshansdorf · DEGoethe University Frankfurt · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although immune checkpoint and targeted therapies offer remarkable benefits for lung cancer treatment, some patients do not qualify for these regimens or do not exhibit consistent benefit. Provided that lung cancer appears to be driven by transforming growth factor beta signaling, we investigated the single drug potency of Pirfenidone, an approved drug for the treatment of lung fibrosis. Five human lung cancer cell lines and one murine line were investigated for transforming growth factor beta inhibition via Pirfenidone by using flow cytometry, In-Cell western analysis, proliferation assays as well as comprehensive analyses of the transcriptome with subsequent bioinformatics analysis. Overall, Pirfenidone induced cell cycle arrest, down-regulated SMAD expression and reduced proliferation in lung cancer. Furthermore, cell stress pathways and pro-apoptotic signaling may be mediated by reduced expression of Survivin. A murine subcutaneous model was used to assess the

Indexed as

immunotherapylung cancerSMADTGFβtumor microenvironment

Identifiers

PMID32039023
PMCPMC6985561
OpenAlexW3003014803

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.