ArticleOncogenesis2014
Glioblastoma cells inhibit astrocytic p53-expression favoring cancer malignancy.
Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 53 citations in OpenAlex.
- Stochastic Nanoscale Biophysical Cues as a Basis for the Induction of Glioblastoma-Like Transcriptional Programs in Astrocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Biomimetic Nanoparticles for Bone Regeneration: Construction Strategies and Therapeutic Mechanisms.International journal of nanomedicine · 2026Review
- Trp53 Deletion Promotes Exacerbated Colitis, Facilitates Lgr5+ Cancer Stem Cell Expansion, and Fuels Tumorigenesis in AOM/DSS-Induced Colorectal Cancer.International journal of molecular sciences · 2024Article
- Co-culture models for investigating cellular crosstalk in the glioma microenvironment.Cancer pathogenesis and therapy · 2024Review
- Extracellular vesicles as modulators of glioblastoma progression and tumor microenvironment.Pathology oncology research : POR · 2024Review
- Understanding Glioblastoma Signaling, Heterogeneity, Invasiveness, and Drug Delivery Barriers.International journal of molecular sciences · 2023Review
- Review
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- Cellular Conversations in Glioblastoma Progression, Diagnosis and Treatment.Cellular and molecular neurobiology · 2023Review
- Protective anti-tumor vaccination against glioblastoma expressing the MHC class II transactivator CIITA.Frontiers in immunology · 2023Article
- Investigational Microbiological Therapy for Glioma.Cancers · 2022Review
- Tumor Microenvironment in Glioma Invasion.Brain sciences · 2022Review
- Glioma: molecular signature and crossroads with tumor microenvironment.Cancer metastasis reviews · 2022Review
- Key Role of Astrocytes in Postnatal Brain and Retinal Angiogenesis.International journal of molecular sciences · 2022Review
- Glioblastoma Microenvironment and Cellular Interactions.Cancers · 2022Review
- Review
- Glioblastoma Microenvironment: From an Inviolable Defense to a Therapeutic Chance.Frontiers in oncology · 2022Review
- The 3.0 Cell Communication: New Insights in the Usefulness of Tunneling Nanotubes for Glioblastoma Treatment.Cancers · 2021Review
- Main genetic differences in high-grade gliomas may present different MR imaging and MR spectroscopy correlates.European radiology · 2021Article
- Glioma Stem-Like Cells and Metabolism: Potential for Novel Therapeutic Strategies.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment has a dynamic and usually cancer-promoting function during all tumorigenic steps. Glioblastoma (GBM) is a fatal tumor of the central nervous system, in which a substantial number of non-tumoral infiltrated cells can be found. Astrocytes neighboring these tumor cells have a particular reactive phenotype and can enhance GBM malignancy by inducing aberrant cell proliferation and invasion. The tumor suppressor p53 has a potential non-cell autonomous function by modulating the expression of secreted proteins that influence neighbor cells. In this work, we investigated the role of p53 on the crosstalk between GBM cells and astrocytes. We show that extracellular matrix (ECM) from p53(+/-) astrocytes is richer in laminin and fibronectin, compared with ECM from p53(+/+) astrocytes. In addition, ECM from p53(+/-) astrocytes increases the survival and the expression of mesenchymal markers in GBM cells, which suggests haploinsufficient phenotype of the p53(+/-) microenvironment. Importantly, conditioned medium from GBM cells blocks the expression of p53 in p53(+/+) astrocytes, even when DNA was damaged. These results suggest that GBM cells create a dysfunctional microenvironment based on the impairment of p53 expression that in turns exacerbates tumor endurance.
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.