Evidence map›Paper›PMID 34376827›Full record

ReviewNature reviews. Cancer2021

Targeting the DNA damage response in immuno-oncology: developments and opportunities.

Roman M Chabanon, Mathieu Rouanne, Christopher J Lord, Jean-Charles Soria, Philippe Pasero, Sophie Postel-Vinay

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
21.8field-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

158 citing papers in PubMed, 1 synthesis or guideline pooled it, 316 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

98 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

6 authors at 4 institutions in 2 countries.

Roman M ChabanonATIP-Avenir Group, Inserm Unit U981, Gustave Roussy Cancer Campus, Université Paris-Saclay, Villejuif, France.ORCID http://orcid.org/0000-0001-5417-3060
Mathieu RouanneEquipe Labellisée Ligue Nationale contre le Cancer, Inserm Unit U1015, Gustave Roussy Cancer Campus, Université Paris-Saclay, Villejuif, France.
Christopher J LordThe CRUK Gene Function Laboratory and Breast Cancer Now Toby Robins Breast Cancer Research Centre, The Institute of Cancer Research, London, UK.ORCID http://orcid.org/0000-0002-3226-0515
Jean-Charles SoriaDrug Development Department (DITEP), Gustave Roussy Cancer Campus, Villejuif, France.
Philippe PaseroEquipe Labellisée Ligue contre le Cancer, Institut de Génétique Humaine, CNRS, Université de Montpellier, Montpellier, France.ORCID http://orcid.org/0000-0001-5891-0822
Sophie Postel-VinayATIP-Avenir Group, Inserm Unit U981, Gustave Roussy Cancer Campus, Université Paris-Saclay, Villejuif, France. sophie.postel-vinay@gustaveroussy.fr.ORCID http://orcid.org/0000-0001-5562-1857
Institute of Cancer Research · GBUniversité Paris-Sud · FRCentre National de la Recherche Scientifique · FRInserm · FR

Funding

Cancer Research UK 24439
6 · The paper itself

Abstract

Immunotherapy has revolutionized cancer treatment and substantially improved patient outcome with regard to multiple tumour types. However, most patients still do not benefit from such therapies, notably because of the absence of pre-existing T cell infiltration. DNA damage response (DDR) deficiency has recently emerged as an important determinant of tumour immunogenicity. A growing body of evidence now supports the concept that DDR-targeted therapies can increase the antitumour immune response by (1) promoting antigenicity through increased mutability and genomic instability, (2) enhancing adjuvanticity through the activation of cytosolic immunity and immunogenic cell death and (3) favouring reactogenicity through the modulation of factors that control the tumour-immune cell synapse. In this Review, we discuss the interplay between the DDR and anticancer immunity and highlight how this dynamic interaction contributes to shaping tumour immunogenicity. We also review the most innovative preclinical approaches that could be used to investigate such effects, including recently developed ex vivo systems. Finally, we highlight the therapeutic opportunities presented by the exploitation of the DDR-anticancer immunity interplay, with a focus on those in early-phase clinical development.

Indexed as

DNA DamageImmunotherapyMedical OncologyAnimalsGenomic InstabilityHumansNeoplasms

Identifiers

PMID34376827
OpenAlexW3187644677

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.