ReviewFrontiers in oncology2019
Temozolomide Induced Hypermutation in Glioma: Evolutionary Mechanisms and Therapeutic Opportunities.
Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed.
- MGMT promoter methylation as a molecular biomarker in neuro-oncology: current practices, challenges, and future directions.Journal of neuro-oncology · 2026Review
- Divergent Roles of Canonical and Non-Canonical Mismatch Repair in Regulating Temozolomide Sensitivity in Glioblastoma.International journal of molecular sciences · 2026Review
- Overcoming Intrinsic and Acquired Temozolomide Resistance in Glioblastoma: Fisetin as a Potential Strategy to Enhance Sensitivity via ZEB1 Modulation.Turkish journal of pharmaceutical sciences · 2026Article
- Immune niche-associated and niche-regulated plasticity in glioblastoma: state transitions, immune escape, and therapeutic vulnerabilities.Frontiers in immunology · 2026Review
- The PIK3CA/AKT pathway drives therapy resistance in rhabdomyosarcoma.Nature communications · 2025Article
- Role of autophagy‑modulating long non‑coding RNAs in tumor radioresistance (Review).Oncology reports · 2025Review
- Immunologic specificity in glioblastoma: Antigen discovery and translational implications.Neuro-oncology advances · 2025Review
- A novel dual-targeting strategy of nanobody-driven protein corona modulation for glioma therapy.Acta pharmaceutica Sinica. B · 2025Article
- Unraveling mutagenic processes influencing the tumor mutational patterns of individuals with constitutional mismatch repair deficiency.Nature communications · 2025Article
- Targeted Polymeric Nanoparticles as a Strategy for the Treatment of Glioblastoma: A Review.Current drug delivery · 2025Review
- AT-0174, a novel dual IDO1/TDO2 enzyme inhibitor, synergises with temozolomide to improve survival in an orthotopic mouse model of glioblastoma.BMC cancer · 2024Article
- Genetic and epigenetic instability as an underlying driver of progression and aggressive behavior in IDH-mutant astrocytoma.Acta neuropathologica · 2024Review
- Review
- Lynch Syndrome-Associated Glioblastoma Treated With Concomitant Chemoradiotherapy and Immune Checkpoint Inhibitors: Case Report and Review of Literature.Brain tumor research and treatment · 2024Article
- A perioperative study of Safusidenib in patients withFuture oncology (London, England) · 2024Article
- Advances in synthetic lethality modalities for glioblastoma multiforme.Open medicine (Warsaw, Poland) · 2024Review
- Individualized Multimodal Immunotherapy for Adults with IDH1 Wild-Type GBM: A Single Institute Experience.Cancers · 2023Article
- Glioma: bridging the tumor microenvironment, patient immune profiles and novel personalized immunotherapy.Frontiers in immunology · 2023Review
- Events in CNS Tumor Pathology Post-2016 WHO CNS: cIMPACT-NOW Updates and Other Advancements: A Comprehensive Review Plus a Summary of the Salient Features of 2021 WHO CNS 5.International journal of general medicine · 2023Review
- Genetic features and therapeutic relevance of emergent circulating tumor DNA alterations in refractory non-colorectal gastrointestinal cancers.Nature communications · 2022Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma are the most common type of malignant brain tumor, with glioblastoma (GBM) representing the most common and most lethal type of glioma. Surgical resection followed by radiotherapy and chemotherapy using the alkylating agent Temozolomide (TMZ) remain the mainstay of treatment for glioma. While this multimodal regimen is sufficient to temporarily eliminate the bulk of the tumor mass, recurrence is inevitable and often poses major challenges for clinical management due to treatment resistance and failure to respond to targeted therapies. Improved tumor profiling capacity has enabled characterization of the genomic landscape of gliomas with the overarching goal to identify clinically relevant subtypes and inform treatment decisions. Increased tumor mutational load has been shown to correlate with higher levels of neoantigens and is indicative of the potential to induce a durable response to immunotherapy. Following treatment with TMZ, a subset of glioma has been identified to recur with increased tumor mutational load. These hypermutant recurrent glioma represent a subtype of recurrence with unique molecular vulnerabilities. In this review, we will elaborate on the current knowledge regarding the evolution of hypermutation in gliomas and the potential therapeutic opportunities that arise with TMZ-induced hypermutation in gliomas.
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.