Evidence map›Paper›PMID 41106370›Full record

ReviewMolecular cell2025

Activation and regulation of cGAS-STING signaling in cancer cells.

Abraham Shim, Yanyang Chen, John Maciejowski

Abstract readReview
In one paragraph

Review in Molecular cell, 2025. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Article
  4. cGAS-STING as a Neuroimmune Traffic Molecule: Unraveling Pathogenic Mechanisms and Therapeutic Potential in Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. 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

3 authors.

Abraham ShimMolecular Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Yanyang ChenMolecular Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
John MaciejowskiMolecular Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: maciejoj@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Investigating Extrachromosomal DNA (ecDNA) Segregation and Repair in CancerR01CA304441 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MACIEJOWSKI, JOHN, SFEIR, AGNEL · 2025 to 2025
$3.2M
Immune control and genomic instability at micronucleiR37CA261183 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JOHN MACIEJOWSKI · 2022 to 2026
$2.4M
Molecular origins and impact of APOBEC3 mutagenesis in cancerR01CA270102 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MACIEJOWSKI, JOHN · 2022 to 2025
$1.9M
Mechanisms of cytosolic DNA degradation by TREX1 in cancer and autoimmune diseaseF31AI181473 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Abraham Shim · 2024 to 2026
$149k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA270102NCI NIH HHS R01 CA304441NCI NIH HHS R37 CA261183NIAID NIH HHS F31 AI181473
6 · The paper itself

Abstract

Genomic instability is a defining feature of cancer that fuels transformation, tumor evolution, and therapeutic resistance. However, genomic instability also incurs an immunological liability by generating cytosolic DNA, a potent trigger of cGAS-STING signaling. In this review, we summarize recent advances in our understanding of the sources of immunostimulatory cytosolic DNA in genomically unstable cancer cells. We examine how newly identified regulatory mechanisms, including chromatin-mediated cGAS suppression, influence the immune-activating potential of cytosolic DNA generated by genomic instability. We also highlight how key regulators, such as the exonuclease TREX1, may be co-opted to shield genomically unstable cancer cells from immune surveillance. By synthesizing these recent advances in our understanding of cGAS-STING activation and regulation in cancer, we aim to highlight emerging therapeutic strategies that leverage cGAS signaling to bolster antitumor immunity.

Indexed as

Membrane ProteinsNeoplasmsNucleotidyltransferasesAnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseExodeoxyribonucleasesGenomic InstabilityHumansPhosphoproteinsSignal TransductionSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseExodeoxyribonucleasesMembrane ProteinsNucleotidyltransferasesPhosphoproteinsSTING1 protein, humanSTING Proteinthree prime repair exonuclease 1autophagycancercGASecDNAgenomic instabilitymicronucleiSTINGTREX1

Identifiers

PMID41106370
PMCPMC12614337

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.