ArticleNeuroscience insights2020
New Cellular Dimensions on Glioblastoma Progression.
Article in Neuroscience insights, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Current status, hotspots and frontiers of ion channel-related research in glioblastoma: a bibliometric analysis from 2005 to 2024.Frontiers in oncology · 2025Review
- Review
- Micro-Vessels-Like 3D Scaffolds for Studying the Proton Radiobiology of Glioblastoma-Endothelial Cells Co-Culture Models.Advanced healthcare materials · 2024Article
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Circadian GeneInternational journal of molecular sciences · 2022Article
- Opposed Interplay between IDH1 Mutations and the WNT/β-Catenin Pathway: Added Information for Glioma Classification.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are brain tumors originated from glial cells. The most frequent form of glioma is the glioblastoma (GB). This lethal tumor is frequently originated from genetic alterations in epidermal growth factor receptor (EGFR) and PI3K pathways. Recent results suggest that signaling pathways, other than primary founder mutations, play a central role in GB progression. Some of these signals are depleted by GB cells from healthy neurons via specialized filopodia known as tumor microtubes (TMs). Here, we discuss the contribution of TMs to vampirize wingless/WNT ligand from neurons. In consequence, wingless/WNT pathway is upregulated in GB to promote tumor progression, and the reduction of these signals in neurons causes the reduction of synapse number and neurodegeneration. These processes contribute to neurological defects and premature death.
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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.