Evidence map›Paper›PMID 41948996›Full record

ArticleOncoimmunology2026

Telomere damage enhances immunogenicity of neuroblastoma and accelerates response to anti-PD-L1 treatment.

Stefanie Höppner, Lisa Werr, Beata Szilagyi, Christoph Bartenhagen, Anna-Maria Hellmann, Carolina Rosswog, Emma Linden, Gerrit Primke, Yvonne Kahlert, Nadliv Ibruli and 5 more

Abstract read
In one paragraph

Article in Oncoimmunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Stefanie HöppnerDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID 0000-0002-2318-1874
Lisa WerrDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Beata SzilagyiDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Christoph BartenhagenDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Anna-Maria HellmannDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Carolina RosswogDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Emma LindenDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Gerrit PrimkeDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Yvonne KahlertDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Nadliv IbruliDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Nadine HemstedtDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Witali LorenzDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Johannes BrägelmannCenter for Molecular Medicine Cologne (CMMC), Faculty of Medicine, University of Cologne, Cologne, Germany.
Michael HölzelInstitute of Experimental Oncology (IEO), Medical Faculty, University Hospital Bonn, University of Bonn, Bonn, Germany.
Matthias FischerDepartment of Experimental Pediatric Oncology and Hematology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomerase is active in the majority of high-risk neuroblastomas, a pediatric tumor associated with poor patient outcomes. In other cancer types, resistance to immune checkpoint blockade was overcome by induction of telomere dysfunction using the telomerase substrate precursor 6-thio-2'-deoxyguanosine (6-thio-dG). Here, we explored whether induction of telomere dysfunction improves the anti-tumor efficacy of immune checkpoint inhibition in neuroblastoma. 6-thio-dG treatment induced the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway and programmed cell death ligand-1 (PD-L1) expression in murine neuroblastoma cells

Indexed as

B7-H1 AntigenImmune Checkpoint InhibitorsNeuroblastomaTelomereAnimalsCell Line, TumorcGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDeoxyguanosineHumansMembrane ProteinsMiceMice, TransgenicN-Myc Proto-Oncogene ProteinNucleotidyltransferasesSTING Proteinalpha-2'-deoxythioguanosineB7-H1 AntigenCD274 protein, humancGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDeoxyguanosineImmune Checkpoint InhibitorsMembrane ProteinsN-Myc Proto-Oncogene ProteinNucleotidyltransferasesSTING ProteinThionucleosidesThionucleotidescGAS-STING pathwaycheckpoint inhibitionimmune cell infiltrationNeuroblastomatelomere damage

Identifiers

PMID41948996
PMCPMC13064559

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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.