ReviewNPJ precision oncology2023
An untapped window of opportunity for glioma: targeting therapy-induced senescence prior to recurrence.
Review in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Aprepitant, a Neurokinin-1 Receptor Antagonist, as a Disruptive Drug for the Treatment of Pediatric Cancer.Journal of clinical medicine · 2026Review
- Integrated biomarker mapping reveals differential expression of senescence profiles in IDH-wild-type glioblastoma recurrent versus primary tumors.Virchows Archiv : an international journal of pathology · 2026Article
- The Emerging Role of Senolytics as a Next-Generation Strategy Against Glioma Recurrence: A Narrative Review.Cancers · 2026Review
- Review
- Temozolomide-induced senescent glioblastoma cells acquire sensitivity to TRAIL death receptor 5-mediated apoptosis.Medical oncology (Northwood, London, England) · 2025Article
- Integrative analysis of single-cell and bulk transcriptome data reveals age-related immune cell alterations in primary glioblastoma associated with prognosis.Cancer immunology, immunotherapy : CII · 2025Article
- Review
- Apoptotic and senolytic effects of hERG/Eag1 channel blockers in combination with temozolomide in human glioblastoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Exploring Multi-Target Therapeutic Strategies for Glioblastoma via Endogenous Network Modeling.International journal of molecular sciences · 2025Article
- Nicotinamide metabolism reprogramming drives reversible senescence of glioblastoma cells.Cellular and molecular life sciences : CMLS · 2025Article
- The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues.Frontiers in cell and developmental biology · 2025Review
- Vagus nerve stimulation: Novel concept for the treatment of glioblastoma and solid cancers by cytokine (interleukin-6) reduction, attenuating the SASP, enhancing tumor immunity.Brain, behavior, & immunity - health · 2024Review
- A brave new framework for glioma drug development.The Lancet. Oncology · 2024Review
- Cell-specific cross-talk proteomics reveals cathepsin B signaling as a driver of glioblastoma malignancy near the subventricular zone.Science advances · 2024Article
- Cerebrospinal fluid D-2-hydroxyglutarate for IDH-mutant glioma monitoring.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 9 institutions in 2 countries.
Funding
Abstract
High-grade gliomas are primary brain tumors that are incredibly refractory long-term to surgery and chemoradiation, with no proven durable salvage therapies for patients that have failed conventional treatments. Post-treatment, the latent glioma and its microenvironment are characterized by a senescent-like state of mitotic arrest and a senescence-associated secretory phenotype (SASP) induced by prior chemoradiation. Although senescence was once thought to be irreversible, recent evidence has demonstrated that cells may escape this state and re-enter the cell cycle, contributing to tumor recurrence. Moreover, senescent tumor cells could spur the growth of their non-senescent counterparts, thereby accelerating recurrence. In this review, we highlight emerging evidence supporting the use of senolytic agents to ablate latent, senescent-like cells that could contribute to tumor recurrence. We also discuss how senescent cell clearance can decrease the SASP within the tumor microenvironment thereby reducing tumor aggressiveness at recurrence. Finally, senolytics could improve the long-term sequelae of prior therapy on cognition and bone marrow function. We critically review the senolytic drugs currently under preclinical and clinical investigation and the potential challenges that may be associated with deploying senolytics against latent glioma. In conclusion, senescence in glioma and the microenvironment are critical and potential targets for delaying or preventing tumor recurrence and improving patient functional outcomes through senotherapeutics.
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.