Evidence map›Paper›PMID 32161398›Full record

ReviewNature reviews. Cancer2020

Inflammatory microenvironment remodelling by tumour cells after radiotherapy.

Martin McLaughlin, Emmanuel C Patin, Malin Pedersen, Anna Wilkins, Magnus T Dillon, Alan A Melcher, Kevin J Harrington

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 529 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
529citing papers in PubMed, 3 pooled it
36.8field-weighted citation impact, top 1% 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

529 citing papers in PubMed, 3 syntheses or guidelines pooled it, 874 citations in OpenAlex.

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  20. Radiation-induced CD200Cellular & molecular immunology · 2026
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469 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Martin McLaughlinTargeted Therapy Team, The Institute of Cancer Research, London, UK. martin.mclaughlin@icr.ac.uk.ORCID http://orcid.org/0000-0002-9739-7133
Emmanuel C PatinTargeted Therapy Team, The Institute of Cancer Research, London, UK.
Malin PedersenTranslational Immunotherapy Team, The Institute of Cancer Research, London, UK.
Anna WilkinsThe Royal Marsden Hospital, London, UK.ORCID http://orcid.org/0000-0002-0425-584X
Magnus T DillonTargeted Therapy Team, The Institute of Cancer Research, London, UK.
Alan A MelcherTranslational Immunotherapy Team, The Institute of Cancer Research, London, UK.
Kevin J HarringtonTargeted Therapy Team, The Institute of Cancer Research, London, UK.
Institute of Cancer Research · GBRoyal Marsden Hospital · GB

Funding

Cancer Research UK 17796Cancer Research UK 28724
6 · The paper itself

Abstract

The development of immune checkpoint inhibitors (ICIs) is revolutionizing the way we think about cancer treatment. Even so, for most types of cancer, only a minority of patients currently benefit from ICI therapies. Intrinsic and acquired resistance to ICIs has focused research towards new combination therapy approaches that seek to increase response rates, the depth of remission and the durability of benefit. In this Review, we describe how radiotherapy, through its immunomodulating effects, represents a promising combination partner with ICIs. We describe how recent research on DNA damage response (DDR) inhibitors in combination with radiotherapy may be used to augment this approach. Radiotherapy can kill cancer cells while simultaneously triggering the release of pro-inflammatory mediators and increasing tumour-infiltrating immune cells - phenomena often described colloquially as turning immunologically 'cold' tumours 'hot'. Here, we focus on new developments illustrating the key role of tumour cell-autonomous signalling after radiotherapy. Radiotherapy-induced tumour cell micronuclei activate cytosolic nucleic acid sensor pathways, such as cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING), and propagation of the resulting inflammatory signals remodels the immune contexture of the tumour microenvironment. In parallel, radiation can impact immunosurveillance by modulating neoantigen expression. Finally, we highlight how tumour cell-autonomous mechanisms might be exploited by combining DDR inhibitors, ICIs and radiotherapy.

Indexed as

Tumor MicroenvironmentAnimalsAntigen PresentationBiomarkers, TumorCaspasesCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDisease SusceptibilityDNA RepairExosomesHumansMembrane ProteinsMolecular Targeted TherapyNeoplasmsNucleotidyltransferasesProtein Processing, Post-TranslationalRadiotherapyBiomarkers, TumorCaspasescGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Protein

Identifiers

PMID32161398
OpenAlexW3011940221

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.