ReviewMolecular neurobiology2022
The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.
Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Therapy enhancing chromosome instability may be advantageous forNAR cancer · 2025Article
- Optimizing Oncolytic Virotherapy for Malignant Glioma: From Bench to Bedside.Cancer management and research · 2025Review
- LINC01094: A key long non-coding RNA in the regulation of cancer progression and therapeutic targets.Heliyon · 2024Review
- Accidental Encounter of Repair Intermediates in Alkylated DNA May Lead to Double-Strand Breaks in Resting Cells.International journal of molecular sciences · 2024Review
- UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.Cellular and molecular life sciences : CMLS · 2024Article
- Nanoparticles for efficient drug delivery and drug resistance in glioma: New perspectives.CNS neuroscience & therapeutics · 2024Review
- Targeting ATR Pathway in Solid Tumors: Evidence of Improving Therapeutic Outcomes.International journal of molecular sciences · 2024Review
- Exposure to Low-Frequency Radiation Changes the Expression of Nestin, VEGF, BCRP and Apoptosis Markers During Glioma Treatment Strategy: AnCurrent radiopharmaceuticals · 2024Article
- Shikonin Induces Glioma Necroptosis, Stemness Decline, and Impedes (Immuno)Proteasome Activity.Stem cells international · 2024Article
- ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer.Frontiers in endocrinology · 2024Review
- Differences in survival prognosticators between children and adults with H3K27M-mutant diffuse midline glioma.CNS neuroscience & therapeutics · 2023Article
- Proteasome Inhibitors against Glioblastoma-Overview of Molecular Mechanisms of Cytotoxicity, Progress in Clinical Trials, and Perspective for Use in Personalized Medicine.Current oncology (Toronto, Ont.) · 2023Review
- Role of Non-Coding RNAs in TGF-β Signalling in Glioma.Brain sciences · 2023Review
- X-ray cross-complementing family: the bridge linking DNA damage repair and cancer.Journal of translational medicine · 2023Review
- Chemical Activation and Mechanical Sensitization of Piezo1 Enhance TRAIL-Mediated Apoptosis in Glioblastoma Cells.ACS omega · 2023Article
- Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity.Scientific reports · 2022Article
- A nanobody-based molecular toolkit for ubiquitin-proteasome system explores the main role of survivin subcellular localization.Frontiers in bioengineering and biotechnology · 2022Article
- Requirements for MRN endonuclease processing of topoisomerase II-mediated DNA damage in mammalian cells.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Gliomas are the most frequent type of tumor in the central nervous system, which exhibit properties that make their treatment difficult, such as cellular infiltration, heterogeneity, and the presence of stem-like cells responsible for tumor recurrence. The response of this type of tumor to chemoradiotherapy is poor, possibly due to a higher repair activity of the genetic material, among other causes. The DNA double-strand breaks are an important type of lesion to the genetic material, which have the potential to trigger processes of cell death or cause gene aberrations that could promote tumorigenesis. This review describes how the different cellular elements regulate the formation of DNA double-strand breaks and their repair in gliomas, discussing the therapeutic potential of the induction of this type of lesion and the suppression of its repair as a control mechanism of brain tumorigenesis.
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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.