ArticleFrontiers in oncology2026
ITPKA suppresses glioma progression and predicts patient prognosis.
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.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Inositol 1,4,5-trisphosphate 3-kinase A (ITPKA) is expressed in various tumors and is associated with tumor progression. This study investigated the expression patterns of ITPKA in gliomas and explored its functional role in glioblastoma (GBM), thereby providing new insights into the diagnostic and prognostic evaluations of ITPKA in this disease. Methods: ITPKA expression levels in glioma tissues of different World Health Organization (WHO) grades and GBM cell lines were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting. U251-MG and T98G cells were transfected with negative control, ITPKA overexpression or ITPKA knockdown plasmids, followed by relevant detections. Subsequently, the viability, proliferation, migration and invasion abilities, cell cycle progression, and apoptosis rate of GBM cells in each group were detected using the Cell-Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) proliferation, wound healing, Transwell, and flow cytometry assays, respectively. Subsequently, the effect of ITPKA on GBM growth was evaluated in a nude mouse subcutaneous tumor xenograft model. Results: Overexpression of ITPKA significantly inhibited the proliferation, migration, and invasion capabilities of GBM cells of the two GBM cell lines Conclusions: Low expression of ITPKA in glioma tissues correlates with GBM progression, indicating that it may act as a tumor suppressor gene and is a candidate biomarker for the molecular diagnostic and prognostic evaluations of glioblastoma.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.