Evidence map›Paper›PMID 29568385›Full record

ArticleOncotarget2018

Persistent DNA strand breaks induce a CAF-like phenotype in normal fibroblasts.

Arnaud J Legrand, Mattia Poletto, Daniela Pankova, Elena Clementi, John Moore, Francesc Castro-Giner, Anderson J Ryan, Eric O'Neill, Enni Markkanen, Grigory L Dianov

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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

10 authors at 4 institutions in 3 countries.

Arnaud J LegrandCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Mattia PolettoCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Daniela PankovaCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Elena ClementiInstitute of Pharmacology and Toxicology, Vetsuisse Faculty, University of Zürich, Zürich 8057, Switzerland.
John MooreCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Francesc Castro-GinerFunctional Genomics Center Zürich, University of Zürich, Zürich 8057, Switzerland.
Anderson J RyanCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Eric O'NeillCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
Enni MarkkanenInstitute of Pharmacology and Toxicology, Vetsuisse Faculty, University of Zürich, Zürich 8057, Switzerland.
Grigory L DianovCRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Department of Oncology, Old Road Campus Research Building, OX37DQ Oxford, UK.
CRUK/MRC Oxford Institute for Radiation Oncology · GBUniversity of Zurich · CHInstitute of Cytology and Genetics · RUUniversity of Oxford · GB

Funding

Cancer Research UK 19277Medical Research Council MC_PC_12002Medical Research Council MC_PC_12006Medical Research Council MC_UU_00001/6
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) are an emerging target for cancer therapy as they promote tumour growth and metastatic potential. However, CAF targeting is complicated by the lack of knowledge-based strategies aiming to selectively eliminate these cells. There is a growing body of evidence suggesting that a pro-inflammatory microenvironment (e.g. ROS and cytokines) promotes CAF formation during tumorigenesis, although the exact mechanisms involved remain unclear. In this study, we reveal that a prolonged pro-inflammatory stimulation causes a

Indexed as

base excision repaircancer-associated fibroblastsmidostaurintumour microenvironmenttumour stroma

Identifiers

PMID29568385
PMCPMC5862606
OpenAlexW2792266826

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.