Evidence map›Paper›PMID 29158317›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2018

An apoptosis-driven 'onco-regenerative niche': roles of tumour-associated macrophages and extracellular vesicles.

Christopher D Gregory, Margaret Paterson

Open access · hybridAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Phosphatidylserine externalization as immune checkpoint in cancer.Pflugers Archiv : European journal of physiology · 2024
    Review
  8. Article
  9. Review
  10. Effects of Therapeutic Hypothermia on Macrophages in Mouse Cochlea Explants.International journal of molecular sciences · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. The Apoptosis Paradox in Cancer.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Review
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

2 authors at 1 institution in 2 countries.

Christopher D GregoryMRC Centre for Inflammation Research, University of Edinburgh College of Medicine and Veterinary Medicine, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK chris.gregory@ed.ac.uk.ORCID http://orcid.org/0000-0002-7553-0132
Margaret PatersonMRC Centre for Inflammation Research, University of Edinburgh College of Medicine and Veterinary Medicine, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
Google (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cell-death programme, apoptosis, is well established as a tumour suppressor mechanism. Paradoxically, high levels of apoptosis in tumours are closely coupled with poor prognosis. Indeed, where it has been studied, cell loss is a striking feature of high-grade cancers, illustrating the importance of considering malignant disease as an imbalance between cell gain and cell loss that favours cell gain rather than as a unidirectional disorder of cell gain alone. In addition to orchestrating cell loss, apoptosis can signal regenerative responses-for example compensatory proliferation-in neighbouring cells. Accumulating evidence suggests that normal tissue repair and regenerative processes are hijacked in the malignant tissue microenvironment such that cancer may be likened to a 'wound that fails to stop repairing'. We have proposed that a critical requirement for the successful growth, progression and re-growth of malignant tumours is a complex milieu, conceptually termed the 'onco-regenerative niche', which is composed, in addition to transformed neoplastic cells, of a network of normal cells and factors activated as if in tissue repair and regeneration. Our work is based around the hypothesis that tumour cell apoptosis, macrophage activation and endothelial activation are key, interlinked elements of the onco-regenerative niche and that apoptotic tumour cell-derived extracellular vesicles provide critical intercellular communication vehicles of the niche. In aggressive B-cell lymphoma, tumour cell apoptosis promotes both angiogenesis and the accumulation of pro-tumour macrophages in the lymphoma microenvironment. Furthermore, apoptotic lymphoma-derived extracellular vesicles have potent pro-tumour potential. These findings have important implications for the roles of apoptosis in regulation of malignant diseases and for the efficacy of apoptosis-inducing anti-cancer therapies.This article is part of the discussion meeting issue 'Extracellular vesicles and the tumour microenvironment'.

Indexed as

ApoptosisExtracellular VesiclesMacrophagesNeoplasmsTumor Microenvironmentapoptosiscancerlymphomamacrophageregenerationrepair

Identifiers

PMID29158317
PMCPMC5717442
OpenAlexW2768627185

What OpenQuestion holds

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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.