Evidence map›Paper›PMID 37692522›Full record

ReviewGenes & diseases2024

Crosstalk between glioblastoma and tumor microenvironment drives proneural-mesenchymal transition through ligand-receptor interactions.

Yancheng Lai, Xiaole Lu, Yankai Liao, Pei Ouyang, Hai Wang, Xian Zhang, Guanglong Huang, Songtao Qi, Yaomin Li

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
8.3field-weighted citation impact, top 2% of its field
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

26 citing papers in PubMed, 29 citations in OpenAlex.

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  13. DUSP8 as a regulator of glioblastoma stem-like cell contribution to tumor vascularization.Journal of experimental & clinical cancer research : CR · 2025
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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

9 authors at 1 institution in 1 country.

Yancheng LaiDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Xiaole LuDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Yankai LiaoDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Pei OuyangDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Hai WangDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Xian ZhangDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Guanglong HuangDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Songtao QiDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Yaomin LiDepartment of Neurosurgery, Institute of Brain Disease, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Nanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common intrinsic and aggressive primary brain tumor in adults, with a median survival of approximately 15 months. GBM heterogeneity is considered responsible for the treatment resistance and unfavorable prognosis. Proneural-mesenchymal transition (PMT) represents GBM malignant progression and recurrence, which might be a breakthrough to understand GBM heterogeneity and overcome treatment resistance. PMT is a complicated process influenced by crosstalk between GBM and tumor microenvironment, depending on intricate ligand-receptor interactions. In this review, we summarize the autocrine and paracrine pathways in the GBM microenvironment and related ligand-receptor interactions inducing PMT. We also discuss the current therapies targeting the PMT-related autocrine and paracrine pathways. Together, this review offers a comprehensive understanding of the failure of GBM-targeted therapy and ideas for future tendencies of GBM treatment.

Indexed as

AutocrineGlioblastomaLigand-receptor interactionMicroenvironmentParacrineProneural-mesenchymal transition

Identifiers

PMID37692522
PMCPMC10491977
OpenAlexW4384831509

What OpenQuestion 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 OpenQuestion graph.