Evidence map›Paper›PMID 38139802›Full record

ReviewPharmaceuticals (Basel, Switzerland)2023

At the Crossroads of the cGAS-cGAMP-STING Pathway and the DNA Damage Response: Implications for Cancer Progression and Treatment.

Tatyana V Korneenko, Nikolay B Pestov, Ivan A Nevzorov, Alexandra A Daks, Kirill N Trachuk, Olga N Solopova, Nickolai A Barlev

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  3. 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
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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

7 authors at 3 institutions in 1 country.

Tatyana V KorneenkoGroup of Cross-Linking Enzymes, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow 117997, Russia.
Nikolay B PestovGroup of Cross-Linking Enzymes, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow 117997, Russia.
Ivan A NevzorovInstitute of Cytology, Tikhoretsky ave 4, St-Petersburg 194064, Russia.ORCID 0000-0002-1224-5772
Alexandra A DaksInstitute of Cytology, Tikhoretsky ave 4, St-Petersburg 194064, Russia.
Kirill N TrachukChumakov Federal Scientific Center for Research and Development of Immune-and-Biological Products, Moscow 108819, Russia.ORCID 0000-0002-2061-0274
Olga N SolopovaResearch Institute of Experimental Diagnostics and Tumor Therapy, Blokhin National Medical Research Center of Oncology, Moscow 115478, Russia.ORCID 0000-0002-5465-6094
Nickolai A BarlevInstitute of Biomedical Chemistry, Moscow 119121, Russia.
Institute of Bioorganic Chemistry · RUInstitute of Cytology · RUSechenov University · RU

Funding

Ministry of Science and Higher Education of the Russian Federation within the framework of state support for the creation and development of World-Class Re-search Centers 'Digital Biodesign and Personalized Healthcare 75-15-2020-913
6 · The paper itself

Abstract

The evolutionary conserved DNA-sensing cGAS-STING innate immunity pathway represents one of the most important cytosolic DNA-sensing systems that is activated in response to viral invasion and/or damage to the integrity of the nuclear envelope. The key outcome of this pathway is the production of interferon, which subsequently stimulates the transcription of hundreds of genes. In oncology, the situation is complex because this pathway may serve either anti- or pro-oncogenic roles, depending on context. The prevailing understanding is that when the innate immune response is activated by sensing cytosolic DNA, such as DNA released from ruptured micronuclei, it results in the production of interferon, which attracts cytotoxic cells to destroy tumors. However, in tumor cells that have adjusted to significant chromosomal instability, particularly in relapsed, treatment-resistant cancers, the cGAS-STING pathway often supports cancer progression, fostering the epithelial-to-mesenchymal transition (EMT). Here, we review this intricate pathway in terms of its association with cancer progression, giving special attention to pancreatic ductal adenocarcinoma and gliomas. As the development of new cGAS-STING-modulating small molecules and immunotherapies such as oncolytic viruses involves serious challenges, we highlight several recent fundamental discoveries, such as the proton-channeling function of STING. These discoveries may serve as guiding lights for potential pharmacological advancements.

Indexed as

BRCAcancercGAMPcGASinterferon signalingmetastasisproton channelSTING

Identifiers

PMID38139802
PMCPMC10747911
OpenAlexW4389223202

What OpenQuestion holds

Textmetadata
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.