SynthesisFrontiers in oncology2022
Ferroptosis in glioma treatment: Current situation, prospects and drug applications.
Synthesis in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 10 citations in OpenAlex.
- Ferroptosis as an immunometabolic checkpoint in brain tumours: spatial vulnerabilities and therapeutic opportunities.Molecular brain · 2026Review
- TAF15-mediated m5C modification of MTHFD2 RNA reveals a novel therapeutic target for IDH mutant gliomas.Biomarker research · 2026Article
- Molecular Effects of Indocyanine Green-Photodynamic Therapy on Programmed Cell Death Pathways in T98G and U-118MG Glioblastoma Cells-An RT-qPCR Study.Current issues in molecular biology · 2026Article
- Targeting Ferroptosis in Glioblastoma: Molecular Mechanisms, Tumor Microenvironment, and Therapeutic Opportunities.Cancers · 2026Review
- From Integrated Analysis to Clinical Insight: ncRNA-Mediated Ferroptosis in Glioblastoma.Cancers · 2026Review
- EF24 targets METTL3 to reprogram m6A methylation and induce ferroptosis: an epitranscriptomic mechanism with therapeutical potential for glioma.Cell communication and signaling : CCS · 2025Article
- Rubidium chloride induces ferroptosis in glioblastoma cells by disrupting glutathione metabolism and redox homeostasis.Cancer cell international · 2025Article
- DNA Damage Repair in Glioblastoma: A Novel Approach to Combat Drug Resistance.Cell proliferation · 2025Article
- Inhibition of miR-9-3p facilitates ferroptosis by activating SAT1/p53 pathway in lung adenocarcinoma.Translational lung cancer research · 2024Article
- Synthesis of carbon dot based Schiff bases and selective anticancer activity in glioma cells.RSC advances · 2024Article
- Research progress on ferroptosis in gliomas (Review).Oncology letters · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a regulatory form of iron-dependent cell death caused by the accumulation of lipid-based reactive oxygen species (ROS) and differs from apoptosis, pyroptosis, and necrosis. Especially in neoplastic diseases, the susceptibility of tumor cells to ferroptosis affects prognosis and is associated with complex effects. Gliomas are the most common primary intracranial tumors, accounting for disease in 81% of patients with malignant brain tumors. An increasing number of studies have revealed the particular characteristics of iron metabolism in glioma cells. Therefore, agents that target a wide range of molecules involved in ferroptosis may regulate this process and enhance glioma treatment. Here, we review the underlying mechanisms of ferroptosis and summarize the potential therapeutic options for targeting ferroptosis in glioma.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.