Evidence map›Paper›PMID 41018101›Full record

ReviewFrontiers in oncology2025

Glioma-neuron interactions: insights from neural plasticity.

Jingyu Feng, Jun Yang

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
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

2 authors.

Jingyu FengDepartment of Neurosurgery, Peking University Third Hospital, Peking University, Beijing, China.
Jun YangDepartment of Neurosurgery, Peking University Third Hospital, Peking University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of gliomas is linked to neuroplasticity. Neurons, which are largely nonregenerative in adulthood, rely on axons and synapses to rebuild the neural network in response to experience and injury. Neural stem cells and immune cells coordinate "creation" (e.g., neurogenesis) and "clearance" (e.g., synaptic pruning), guided by signals from neural circuits. This review summarizes neuroplasticity mechanisms and explores their connection to gliomas, revealing that glioma cells hijack neural network derived signals to promote growth, migration, and stem-like properties, while simultaneously disrupting normal neural conduction. Similar to oligodendrocyte precursor cells (OPCs), gliomas exploit neural network regulation but are prone to uncontrolled proliferation. Moreover, glioma induced neural hyperexcitability disrupts circuit homeostasis, creating a permissive microenvironment for glioma progression. Consequently, neuroplasticity will contribute to the study of glioma related mechanisms and the development of more targeted strategies for prevention and control.

Indexed as

gliomaglioma stem cellmigrationneural mechanismsneural networksneuroplasticitytumorigenesistumor microenvironment

Identifiers

PMID41018101
PMCPMC12460145

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.