Evidence map›Paper›PMID 36923251›Full record

ReviewFrontiers in cell and developmental biology2023

Roles of STAT3 in the pathogenesis and treatment of glioblastoma.

Weijia Fu, Xue Hou, Lihua Dong, Wei Hou

Open access · goldFull text readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
15.9field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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  15. The CHI3L1 protein plays role as a protecting factor against autophagy in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2026
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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

4 authors at 2 institutions in 1 country.

Weijia FuDepartment of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
Xue HouDepartment of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
Lihua DongDepartment of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
Wei HouDepartment of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most malignant of astrocytomas mainly involving the cerebral hemispheres and the cerebral cortex. It is one of the fatal and refractory solid tumors, with a 5-year survival rate of merely 5% among the adults. IL6/JAK/STAT3 is an important signaling pathway involved in the pathogenesis and progression of GBM. The expression of STAT3 in GBM tissues is substantially higher than that of normal brain cells. The abnormal activation of STAT3 renders the tumor microenvironment of GBM immunosuppression. Besides, blocking the STAT3 pathway can effectively inhibit the growth and metastasis of GBM. On this basis, inhibition of STAT3 may be a new therapeutic approach for GBM, and the combination of STAT3 targeted therapy and conventional therapies may improve the current status of GBM treatment. This review summarized the roles of STAT3 in the pathogenesis of GBM and the feasibility of STAT3 for GBM target therapy.

Indexed as

combination therapyglioblastomaradiotherapystat3targeted therapy

Identifiers

PMID36923251
PMCPMC10009693
OpenAlexW4322504329

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read19
reference markers read6
identifiers read2
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.