Evidence map›Paper›PMID 38214828›Full record

ArticleJournal of neuro-oncology2024

Investigating the effects of PTEN mutations on cGAS-STING pathway in glioblastoma tumours.

Eda Dogan, Zafer Yildirim, Taner Akalin, Erkin Ozgiray, Nevhis Akinturk, Cagdas Aktan, Asli Ece Solmaz, Huseyin Biceroglu, Kadri Emre Caliskan, Yesim Ertan and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

13 authors at 2 institutions in 1 country.

Eda Dogan *Department of Medical Biology, Ege University Faculty of Medicine, Izmir, Türkiye.
Zafer Yildirim *Department of Medical Biology, Ege University Faculty of Medicine, Izmir, Türkiye.
Taner AkalinDepartment of Pathology, Ege University Faculty of Medicine, Izmir, Türkiye.
Erkin OzgirayDepartment of Neurosurgery, Ege University Faculty of Medicine, Izmir, Türkiye.
Nevhis AkinturkDepartment of Neurosurgery, Ege University Faculty of Medicine, Izmir, Türkiye.
Cagdas AktanDepartment of Medical Biology, Beykent University School of Medicine, İstanbul, Türkiye.
Asli Ece SolmazDepartment of Medical Genetics, Ege University Faculty of Medicine, Izmir, Türkiye.
Huseyin BicerogluDepartment of Neurosurgery, Ege University Faculty of Medicine, Izmir, Türkiye.
Kadri Emre CaliskanDepartment of Neurosurgery, Ege University Faculty of Medicine, Izmir, Türkiye.
Yesim ErtanDepartment of Pathology, Ege University Faculty of Medicine, Izmir, Türkiye.
Taskin YurtsevenDepartment of Neurosurgery, Ege University Faculty of Medicine, Izmir, Türkiye.
Buket KosovaDepartment of Medical Biology, Ege University Faculty of Medicine, Izmir, Türkiye.
Vildan BozokDepartment of Medical Biology, Ege University Faculty of Medicine, Izmir, Türkiye. vldnbozok@gmail.com.ORCID http://orcid.org/0000-0003-3915-6363
Ege University · TRBeykent University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPTEN is a tumour suppressor gene and well-known for being frequently mutated in several cancer types. Loss of immunogenicity can also be attributed to PTEN loss, because of its role in establishing the tumour microenvironment. Therefore, this study aimed to represent the link between PTEN and cGAS-STING activity, a key mediator of inflammation, in tumour samples of glioblastoma patients.

methodsTumour samples of 36 glioblastoma patients were collected. After DNA isolation, all coding regions of PTEN were sequenced and analysed. PTEN expression status was also evaluated by qRT-PCR, western blot, and immunohistochemical methods. Interferon-stimulated gene expressions, cGAMP activity, CD8 infiltration, and Granzyme B expression levels were determined especially for the evaluation of cGAS-STING activity and immunogenicity.

resultsMutant PTEN patients had significantly lower PTEN expression, both at mRNA and protein levels. Decreased STING, IRF3, NF-KB1, and RELA mRNA expressions were also found in patients with mutant PTEN. Immunohistochemistry staining of PTEN displayed expressional loss in 38.1% of the patients. Besides, patients with PTEN loss had considerably lower amounts of IFNB and IFIT2 mRNA expressions. Furthermore, CD8 infiltration, cGAMP, and Granzyme B levels were reduced in the PTEN loss group.

conclusionThis study reveals the immunosuppressive effects of PTEN loss in glioblastoma tumours via the cGAS-STING pathway. Therefore, determining the PTEN status in tumours is of great importance, like in situations when considering the treatment of glioblastoma patients with immunotherapeutic agents.

Indexed as

GlioblastomaGranzymesHumansMutationNucleotidyltransferasesPTEN PhosphohydrolaseRNA, MessengerTumor MicroenvironmentGranzymesNucleotidyltransferasesPTEN PhosphohydrolasePTEN protein, humanRNA, MessengercGAS-STING pathwayGlioblastomaImmunogenicityInterferon responsePTEN

Identifiers

PMID38214828
PMCPMC10834568
OpenAlexW4390789414

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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.