ArticleJournal of oncology2012
Glioma revisited: from neurogenesis and cancer stem cells to the epigenetic regulation of the niche.
Article in Journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 58 citations in OpenAlex.
- Butyl and isobutyl ortho-coumaric acid derivatives reduce self-renewal and MGMT expression in GBM cells with stem cell-like characteristicsBiomolecules & biomedicine · 2026Article
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- Review
- Modular Hub Genes in DNA Microarray Suggest Potential Signaling Pathway Interconnectivity in Various Glioma Grades.Biology · 2024Article
- Deciphering Glioblastoma: Fundamental and Novel Insights into the Biology and Therapeutic Strategies of Gliomas.Current issues in molecular biology · 2024Review
- Metabotropic Glutamate Receptors Type 3 and 5 Feature the "NeuroTransmitter-type" of Glioblastoma: A Bioinformatic Approach.Current neuropharmacology · 2024Article
- Aloe-Emodin Overcomes Anti-Cancer Drug Resistance to Temozolomide and Prevents Colony Formation and Migration in Primary Human Glioblastoma Cell Lines NULU and ZAR.Molecules (Basel, Switzerland) · 2023Article
- Expression of CD133 Cancer Stem Cell Marker in IDH-Mutant and IDH-wildtype (Isocitrate Dehydrogenase) Astrocytoma.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Targeted inhibition of ubiquitin signaling reverses metabolic reprogramming and suppresses glioblastoma growth.Communications biology · 2022Article
- Fibroblast growth factor 2 is a druggable target against glioblastoma: A computational investigation.Frontiers in chemistry · 2022Article
- Runx1 promotes the development of glioma cells by regulating JAK-STAT signalling pathway.Archives of medical science : AMS · 2022Article
- Targeting Protein Kinase C in Glioblastoma Treatment.Biomedicines · 2021Review
- Article
- Review
- Characterization of primary glioma cell lines derived from the patients according to 2016 CNS tumour WHO classification and comparison with their parental tumours.Journal of neuro-oncology · 2021Article
- Implication of Lactucopicrin in Autophagy, Cell Cycle Arrest and Oxidative Stress to Inhibit U87Mg Glioblastoma Cell Growth.Molecules (Basel, Switzerland) · 2020Article
- Expression and pharmacological inhibition of TrkB and EGFR in glioblastoma.Molecular biology reports · 2020Article
- Exploring Notch Pathway to Elucidate Phenotypic Plasticity and Intra-tumor Heterogeneity in Gliomas.Scientific reports · 2019Article
- Bmi1 regulates human glioblastoma stem cells through activation of differential gene networks in CD133+ brain tumor initiating cells.Journal of neuro-oncology · 2019Article
- Interaction of hematopoietic CD34+ CD45+ stem cells and cancer cells stimulated by TGF‑β1 in a model of glioblastoma in vitro.Oncology reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are the most incident brain tumor in adults. This malignancy has very low survival rates, even when combining radio- and chemotherapy. Among the gliomas, glioblastoma multiforme (GBM) is the most common and aggressive type, and patients frequently relapse or become refractory to conventional therapies. The fact that such an aggressive tumor can arise in such a carefully orchestrated organ, where cellular proliferation is barely needed to maintain its function, is a question that has intrigued scientists until very recently, when the discovery of the existence of proliferative cells in the brain overcame such challenges. Even so, the precise origin of gliomas still remains elusive. Thanks to new advents in molecular biology, researchers have been able to depict the first steps of glioma formation and to accumulate knowledge about how neural stem cells and its progenitors become gliomas. Indeed, GBM are composed of a very heterogeneous population of cells, which exhibit a plethora of tumorigenic properties, supporting the presence of cancer stem cells (CSCs) in these tumors. This paper provides a comprehensive analysis of how gliomas initiate and progress, taking into account the role of epigenetic modulation in the crosstalk of cancer cells with their environment.
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.