ArticleOncology letters2017
Identification of potential therapeutic targets for gliomas by bioinformatics analysis.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 5 citations in OpenAlex.
- ITPKA suppresses glioma progression and predicts patient prognosis.Frontiers in oncology · 2026Article
- Exploration of the radiosensitivity-related prognostic risk signature in patients with glioma: evidence from microarray data.Journal of translational medicine · 2023Article
- ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.Aging · 2021Article
- Identification of hub genes and pathways in glioblastoma by bioinformatics analysis.Oncology letters · 2019Article
- Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma.Biological research · 2018Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are primary tumors that originate in the brain or spinal cord and develop from supportive glial cells. The present study aimed to identify potential candidate molecular markers for the treatment of gliomas, and to explore the underlying mechanisms of this disease. The gene expression profile data GSE50021, which consisted of 10 specimens of normal brain tissues and 35 specimens of glioma tissues, was downloaded from Gene Expression Omnibus (GEO). The methylation microarray data GSE50022, consisting of 28 glioma specimens, was also downloaded from GEO. Differentially expressed genes (DEGs) between patients with glioma and normal individuals were identified, and key methylation sites were screened. Transcriptional regulatory networks were constructed, and target genes were selected. Survival analysis of key methylation sites and risk analysis of sub-pathways were performed, from which key genes and pathways were selected. A total of 79 DEGs and 179 key methylation sites were identified, of which 20 target genes and 36 transcription factors were included in the transcriptional regulatory network. Glutamate metabotropic receptor 2 (
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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 OpenQuestion graph.