Evidence map›Paper›PMID 37475576›Full record

ReviewCancer science2023

Targeting the loss of cGAS/STING signaling in cancer.

Nobunari Sasaki, Mizuki Homme, Shunsuke Kitajima

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.1field-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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Therapeutic targeting of the cGAS-STING pathway in human disease.The Journal of clinical investigation · 2026
    Review
  3. Article
  4. Review
  5. Article
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  7. Review
  8. Article
  9. Article
  10. Conjugated STING agonists.Molecular therapy. Nucleic acids · 2025
    Review
  11. Review
  12. Review
  13. Article
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  15. Review
  16. Review
  17. Article
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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

3 authors at 1 institution in 1 country.

Nobunari SasakiDepartment of Cell Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Mizuki HommeDepartment of Cell Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Shunsuke KitajimaDepartment of Cell Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0001-6532-2543
Japanese Foundation For Cancer Research · JP

Funding

Astellas Foundation for Research on Metabolic DisordersDaiichi Sankyo Foundation of Life ScienceJapan Science and Technology Agency JPMJFR215YJapan Society for the Promotion of Science 20H03521Japan Society for the Promotion of Science 22K19467Kato Memorial Bioscience FoundationKobayashi Foundation for Cancer ResearchMSD Life Science Foundation, Public Interest Incorporated FoundationNaito FoundationPrincess Takamatsu Cancer Research FundTakeda Science FoundationVehicle Racing Commemorative Foundation
6 · The paper itself

Abstract

The cGAS/STING pathway provides a key host defense mechanism by detecting the accumulation of cytoplasmic double-stranded DNA (dsDNA) and mediating innate and adaptive immune signaling. In addition to detecting pathogen-derived dsDNA, cGAS senses intrinsic dsDNA, such as those associated with defective cell cycle progression and mitophagy that has leaked from the nucleus or mitochondria, and subsequently evokes host immunity to eliminate pathogenic cells. In cancer cells, dysregulation of DNA repair and cell cycle caused at the DNA replication checkpoint and spindle assembly checkpoint results in aberrant cytoplasmic dsDNA accumulation, stimulating anti-tumor immunity. Therefore, the suppression of cGAS/STING signaling is beneficial for survival and frequently observed in cancer cells as a way to evade detection by the immune system, and is likely to be related to immune checkpoint blockade (ICB) resistance. Indeed, the mechanisms of ICB resistance overlap with those acquired in cancers during immunoediting to evade immune surveillance. This review highlights the current understanding of cGAS/STING suppression in cancer cells and discusses how to establish effective strategies to regenerate effective anti-tumor immunity through reactivation of the cGAS/STING pathway.

Indexed as

Membrane ProteinsNeoplasmsNucleotidyltransferasesSignal TransductionAnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA RepairHumansImmune Checkpoint InhibitorsSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseImmune Checkpoint InhibitorsMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Proteinanti-tumor immunitycGASDNA-damaging agentepigenetic inhibitorSTING

Identifiers

PMID37475576
PMCPMC10551601
OpenAlexW4384924971

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.