ReviewCancers2021
One-Carbon Metabolism Associated Vulnerabilities in Glioblastoma: A Review.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 18 citations in OpenAlex.
- Construction and validation of a folate metabolism-related gene signature for prognosis prediction, immune landscape characterization, and molecular subtyping in glioma.Cancer causes & control : CCC · 2026Article
- TAF15-mediated m5C modification of MTHFD2 RNA reveals a novel therapeutic target for IDH mutant gliomas.Biomarker research · 2026Article
- Review
- Dissecting the Dual Drug Candidates Against Glioblastoma and Oligodendroglioma Through Integrated Transcriptome Analysis and Virtual Screening.Cell biochemistry and biophysics · 2025Article
- Theranostic Potential of Copper-64 ATSM Targeting MTHFD2: An In Silico Perspective on Hypoxia-Selective Imaging and Therapy.Cell biochemistry and biophysics · 2025Article
- From Biomarker Discovery to Clinical Applications of Metabolomics in Glioblastoma.Metabolites · 2025Review
- Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance.Frontiers in cell and developmental biology · 2025Review
- MAT2a and AHCY inhibition disrupts antioxidant metabolism and reduces glioblastoma cell survival.bioRxiv : the preprint server for biology · 2024Article
- Glutaminolysis is associated with mitochondrial pathway activation and can be therapeutically targeted in glioblastoma.Cancer & metabolism · 2024Article
- The Pivotal Role of One-Carbon Metabolism in Neoplastic Progression During the Aging Process.Biomolecules · 2024Review
- One-carbon-mediated purine synthesis underlies temozolomide resistance in glioblastoma.Cell death & disease · 2024Article
- Metabolic Reprogramming in Glioblastoma Multiforme: A Review of Pathways and Therapeutic Targets.Cells · 2024Review
- MGMT ProFWise: Unlocking a New Application for Combined Feature Selection and the Rank-Based Weighting Method to Link MGMT Methylation Status to Serum Protein Expression in Patients with Glioblastoma.International journal of molecular sciences · 2024Article
- MTAP loss: a possible therapeutic approach for glioblastoma.Journal of translational medicine · 2022Review
- Rewired Metabolism of Amino Acids and Its Roles in Glioma Pathology.Metabolites · 2022Review
- Review
- Novel Treatment Strategies for Glioblastoma-A Summary.Cancers · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Altered cell metabolism is a hallmark of cancer cell biology, and the adaptive metabolic strategies of cancer cells have been of recent interest to many groups. Metabolic reprogramming has been identified as a critical step in glial cell transformation, and the use of antimetabolites against glioblastoma has been investigated. One-carbon (1-C) metabolism and its associated biosynthetic pathways, particularly purine nucleotide synthesis, are critical for rapid proliferation and are altered in many cancers. Purine metabolism has also been identified as essential for glioma tumourigenesis. Additionally, alterations of 1-C-mediated purine synthesis have been identified as commonly present in brain tumour initiating cells (BTICs) and could serve as a phenotypic marker of cells responsible for tumour recurrence. Further research is required to elucidate mechanisms through which metabolic vulnerabilities may arise in BTICs and potential ways to therapeutically target these metabolic processes. This review aims to summarize the role of 1-C metabolism-associated vulnerabilities in glioblastoma tumourigenesis and progression and investigate the therapeutic potential of targeting this pathway in conjunction with other treatment strategies.
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.