Evidence map›Paper›PMID 41624425›Full record

ArticleNeuro-oncology advances

Increased immunogenicity of hypermutated SB28 syngeneic glioblastoma is partially mediated by alterations in tumor chemokine expression.

Kevin Thomas Breen, Tuesday Haynes, Matthew Bryce Watowich, Seketoulie Keretsu, Aiguo Li, Yongmei Zhao, Wei Zhang, Meili Zhang, Hua Song, Nicole Briceno and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology advances. 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

14 authors.

Kevin Thomas BreenLaboratory of Integrative Cancer Immunology, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.ORCID https://orcid.org/0009-0007-3998-3920
Tuesday HaynesNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Matthew Bryce WatowichNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Seketoulie KeretsuLaboratory of Integrative Cancer Immunology, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Aiguo LiNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Yongmei ZhaoCCR-SF Bioinformatics Group, Bioinformatics and Computational Science Directorate, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA.
Wei ZhangNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Meili ZhangNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Hua SongNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Nicole BricenoNational Human Genome Research Institute, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Dionne DavisNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Masashi WatanabeLaboratory of Cancer Biology and Genetics, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Mark Richard GilbertNeuro-Oncology Branch, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Masaki TerabeLaboratory of Integrative Cancer Immunology, CCR, NCI, National Institutes of Health, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0002-1777-0189

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Glioblastoma (GBM) prognosis remains poor, and although immune checkpoint inhibitors (ICI) have transformed the treatment of many tumors, they are ineffective in GBM. However, response to ICIs occurs in high-tumor-mutational-burden (TMB) GBMs. To address the immunological impact of high TMB in GBM, we created a high TMB syngeneic mouse model from the low TMB SB28 GBM cell line. Methods: We used CRISPR-Cas9 to target murine Results: Loss of mismatch repair (MMR) proteins Msh2 or Mlh1 increased nonsynonymous mutations. A fraction of mice with intracranial Conclusion: Mismatch repair-deficient SB28 tumors were more immunogenic, but this was not completely correlated with TMB. Rather, rejection depended on increased secretion of pro-inflammatory chemokines.

Indexed as

checkpoint inhibitorglioblastomaimmunotherapymismatch repair genestumor mutational burden

Identifiers

PMID41624425
PMCPMC12859701

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.