Evidence map›Paper›PMID 42109665›Full record

ArticleFrontiers in oncology2026

Glia-derived VCAM1 promotes glioma progression.

Jiajing Dai, Hailong Zheng, Jiaxu Luo, Minlin Dai, Xiao-Ling Hu, Wenzhi Sun

Abstract read
In one paragraph

Article in Frontiers in oncology, 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

6 authors.

Jiajing Dai *Department of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.
Hailong Zheng *Department of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.
Jiaxu Luo *Department of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.
Minlin DaiDepartment of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.
Xiao-Ling HuDepartment of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.
Wenzhi SunDepartment of Neurobiology, Basic Medical Sciences, Capital Medical University School, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The dynamic interactions between glioma cells and the tumor microenvironment (TME) drive tumor progression and therapeutic resistance. VCAM1 is known to facilitate tumor metastasis in various cancers; however, its specific function in the glioma microenvironment remains poorly defined. Methods: To elucidate VCAM1's role in glioma, we evaluated its expression in human glioma datasets and correlated it with patient survival outcomes. Using syngeneic and primary mouse glioma models, we characterized VCAM1 expression in tumor and stromal cell populations. Furthermore, we selectively ablated VCAM1 in GLAST-positive astrocytes in a glioma-bearing mouse model to evaluate its functional impact on tumor growth and overall survival. Results: We identified that VCAM1 is highly enriched in proliferative glioma stem cell-like cells (GSLCs); for example, 86.5% of SOX2 Conclusion: Astrocyte-derived VCAM1 is a critical driver of glioma progression, mediating essential interactions between tumor cells and the TME. Targeting VCAM1 signaling presents a promising, microenvironment-focused therapeutic strategy, though its clinical application must account for regional and genetic tumor heterogeneity.

Indexed as

astrocytegliomaglioma stem cell-like cellstherapeutic targetVCAM1

Identifiers

PMID42109665
PMCPMC13152763

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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.