Evidence map›Paper›PMID 39544936›Full record

ReviewFrontiers in immunology2024

Genomic instability as a driver and suppressor of anti-tumor immunity.

Marta Requesens, Floris Foijer, Hans W Nijman, Marco de Bruyn

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

4 authors.

Marta RequesensDepartment of Obstetrics and Gynecology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Floris FoijerEuropean Research Institute for the Biology of Ageing, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Hans W NijmanDepartment of Obstetrics and Gynecology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Marco de BruynDepartment of Obstetrics and Gynecology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability is a driver and accelerator of tumorigenesis and influences disease outcomes across cancer types. Although genomic instability has been associated with immune evasion and worsened disease prognosis, emerging evidence shows that genomic instability instigates pro-inflammatory signaling and enhances the immunogenicity of tumor cells, making them more susceptible to immune recognition. While this paradoxical role of genomic instability in cancer is complex and likely context-dependent, understanding it is essential for improving the success rates of cancer immunotherapy. In this review, we provide an overview of the underlying mechanisms that link genomic instability to pro-inflammatory signaling and increased immune surveillance in the context of cancer, as well as discuss how genomically unstable tumors evade the immune system. A better understanding of the molecular crosstalk between genomic instability, inflammatory signaling, and immune surveillance could guide the exploitation of immunotherapeutic vulnerabilities in cancer.

Indexed as

Genomic InstabilityNeoplasmsAnimalsHumansImmunologic SurveillanceImmunotherapySignal TransductionTumor EscapeTumor MicroenvironmentcGAS-STINGchromosomal instabilitygenomic instabilityimmune evasionMMRdtumor-infiltrating lymphocytes

Identifiers

PMID39544936
PMCPMC11562473

What OpenQuestion holds

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Registered trials

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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.