Evidence map›Paper›PMID 42211393›Full record

ArticleNeuro-oncology advances

Inhibition of chemokine CXCL12 modulates the tumor microenvironment in glioblastoma and potentiates immune checkpoint inhibitor efficacy in a tissue-specific manner.

Chen Makranz, Caitlin Huguely, Meili Zhang, Dionne Davis, Brita Anderson, Tuesday Haynes, Jo Spurgeon, Ayaka Hara, Nicole Briceno, Hua Song and 5 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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Chen MakranzNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Caitlin HuguelyNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Meili ZhangNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Dionne DavisNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Brita AndersonNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Tuesday HaynesNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Jo SpurgeonLaboratory of Integrative Cancer Immunology, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Ayaka HaraLaboratory of Integrative Cancer Immunology, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Nicole BricenoCenter for Precision Health Research, National Human Genome Research Institute, NIH, Bethesda, Maryland, USA.
Hua SongNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Wei ZhangNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Hideho OkadaDepartment of Neurological Surgery, UCSF, San Francisco, California, USA.ORCID https://orcid.org/0000-0003-0076-9920
Masashi WatanabeNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Mark R GilbertNeuro-Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Masaki TerabeLaboratory of Integrative Cancer Immunology, National Cancer Institute, NIH, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0002-1777-0189

Funding

Preclinical development of breakthrough immunotherapy for brain tumorsR35NS142982 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Hideho Okada · 2026 to 2026
$943k
NINDS NIH HHS R35 NS142982
6 · The paper itself

Abstract

Background: Immunotherapy, while effective for many extra-cranial solid tumors, has not shown benefits against glioblastoma. Limited T cell infiltration and an immunosuppressive tumor microenvironment (TME) are among the main barriers to successful immunotherapy. We hypothesized that blocking the chemokine CXCL12 would modulate the TME composition and reverse GBM resistance to immunotherapy. Methods: We used a syngeneic murine SB28 GBM model resistant to immune checkpoint inhibitor (ICI) and compared orthotopic and subcutaneous tumors to differentiate tumor-intrinsic factors from CNS-related barriers. We treated SB28 tumor-bearing mice with vehicle, ICI, CXCL12 inhibitor (NOX-A12), or a combination of NOX-A12 with ICI. We assessed treatment effects on immune cell populations in the blood and the TME, and on tumor growth and mouse survival. Results: ICI alone increased effector CD8 Conclusion: CXCL12 inhibition demonstrates therapeutic potential in facilitating anti-tumor immune response by dual mechanism, including T cell expansion and TAM reduction. The inability to deplete TAMs and improve survival in intracranial GBM underscores the need to address brain-specific mechanisms underlying TAM persistence to advance immunotherapy in GBM.

Indexed as

chemokine CXCL12glioblastomaimmune checkpoint inhibitorstumor-associated macrophagestumor microenvironment

Identifiers

PMID42211393
PMCPMC13215089

What OpenQuestion holds

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Read underepoch 390

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.