ReviewCancers2021
Residual Disease in Glioma Recurrence: A Dangerous Liaison with Senescence.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 34 citations in OpenAlex.
- Glioblastoma recurrence: An NGS-centered seed-soil framework.Neoplasia (New York, N.Y.) · 2026Article
- Glioblastoma: epidemiology, molecular pathogenesis, diagnosis, management, and therapeutic resistance.Molecular biomedicine · 2026Review
- Beyond Resection: Surgery as an Evolutionary Bottleneck Shaping Tumor Evolution and Treatment Response in Diffuse Gliomas.Cancers · 2026Review
- Towards a personalized perspective on gliomas: an epigenetic-immuno-inflammatory aging framework.Frontiers in immunology · 2026Review
- Extracellular matrix stiffness conditions glioblastoma cells for long-term migration: Mechanical memory as a driver of invasion and recurrence in glioblastoma.Neuro-oncology · 2026Review
- Review
- Bioresponsive Hyaluronic Acid-Based Hydrogel Inhibits Matrix Metalloproteinase-2 in Glioblastoma Microenvironment.ChemMedChem · 2025Article
- EIF2S2 as a prognostic marker and therapeutic target in glioblastoma: insights into its role and downstream mechanisms.Cancer cell international · 2025Article
- Comparative Clinical-Imaging and Histogenetic Analysis Between Astrocytoma IDH-Mutant Grade 4 and Glioblastoma IDH-Wildtype-Is There Really a Worse One?Diagnostics (Basel, Switzerland) · 2025Article
- Immunotherapeutic advances in glioma management: The rise of vaccine-based approaches.CNS neuroscience & therapeutics · 2024Review
- Optical Methods for Brain Tumor Detection: A Systematic Review.Journal of clinical medicine · 2024Review
- VC-resist glioblastoma cell state: vessel co-option as a key driver of chemoradiation resistance.Nature communications · 2024Article
- Intrinsic and Microenvironmental Drivers of Glioblastoma Invasion.International journal of molecular sciences · 2024Review
- Modelling the dynamics of senescence spread.Aging cell · 2023Article
- Review
- Analysis and validation of aging-related genes in prognosis and immune function of glioblastoma.BMC medical genomics · 2023Article
- Review
- Re-purposing the pro-senescence properties of doxorubicin to introduce immunotherapy in breast cancer brain metastasis.Cell reports. Medicine · 2022Article
- CD44 Depletion in Glioblastoma Cells Suppresses Growth and Stemness and Induces Senescence.Cancers · 2022Article
- Article
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 1 institution in 1 country.
Funding
Abstract
With a dismally low median survival of less than two years after diagnosis, Glioblastoma (GBM) is the most lethal type of brain cancer. The standard-of-care of surgical resection, followed by DNA-damaging chemo-/radiotherapy, is often non-curative. In part, this is because individual cells close to the resection border remain alive and eventually undergo renewed proliferation. These residual, therapy-resistant cells lead to rapid recurrence, against which no effective treatment exists to date. Thus, new experimental approaches need to be developed against residual disease to prevent GBM survival and recurrence. Cellular senescence is an attractive area for the development of such new approaches. Senescence can occur in healthy cells when they are irreparably damaged. Senescent cells develop a chronic secretory phenotype that is generally considered pro-tumorigenic and pro-migratory. Age is a negative prognostic factor for GBM stage, and, with age, senescence steadily increases. Moreover, chemo-/radiotherapy can provide an additional increase in senescence close to the tumor. In light of this, we will review the importance of senescence in the tumor-supportive brain parenchyma, focusing on the invasion and growth of GBM in residual disease. We will propose a future direction on the application of anti-senescence therapies against recurrent GBM.
Indexed as
Identifiers
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.