ReviewGlia2011
Drosophila melanogaster as a model system for human brain cancers.
Review in Glia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 89 citations in OpenAlex.
- Long-Read Transcriptome Sequencing and Functional Validation Reveals Novel and Oncogenic Gene Fusions in Fusion Panel-Negative Gliomas.bioRxiv : the preprint server for biology · 2026Article
- Bridging the Gap: How Organ-on-a-Chip Technology Facilitates the Battle against Glioma.Small science · 2026Review
- EyaHOST, a modular genetic system for investigation of intercellular and tumor-host interactions in Drosophila melanogaster.Cell reports methods · 2025Article
- Transcriptome-Wide Analysis of Brain Cancer Initiated by Polarity Disruption inInternational journal of molecular sciences · 2025Article
- Drosophila melanogaster as a Model System for Human Glioblastoma.Advances in experimental medicine and biology · 2025Review
- Article
- Speeding up Glioblastoma Cancer Research: Highlighting the Zebrafish Xenograft Model.International journal of molecular sciences · 2024Review
- Ribogenesis boosts controlled by HEATR1-MYC interplay promote transition into brain tumour growth.EMBO reports · 2024Article
- Co-dependent regulation of p-BRAF and potassium channel KCNMA1 levels drives glioma progression.Cellular and molecular life sciences : CMLS · 2023Article
- Synaptic components are required for glioblastoma progression in Drosophila.PLoS genetics · 2022Article
- Expression of the Human Serotonin 5-HTCells · 2022Article
- Review
- Article
- V-ATPase controls tumor growth and autophagy in a Drosophila model of gliomagenesis.Autophagy · 2021Article
- Insulin signaling mediates neurodegeneration in glioma.Life science alliance · 2021Article
- Cell-to-cell communication mediates glioblastoma progression inBiology open · 2020Article
- Sequential Ras/MAPK and PI3K/AKT/mTOR pathways recruitment drives basal extrusion in the prostate-like gland of Drosophila.Nature communications · 2020Article
- Tep1 Regulates Yki Activity in Neural Stem Cells inFrontiers in cell and developmental biology · 2020Article
- Glioblastoma cells vampirize WNT from neurons and trigger a JNK/MMP signaling loop that enhances glioblastoma progression and neurodegeneration.PLoS biology · 2019Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Glioblastomas (GBM), the most common primary brain tumors, infiltrate the brain, grow rapidly, and are refractory to current therapies. Signature genetic lesions in glioblastomas include mutation of the epidermal growth factor receptor tyrosine kinase (EGFR) receptor tyrosine kinase and activating mutations in components of the PI-3 kinase (PI3K) pathway. Despite years of study, how these pathways specifically regulate glial pathogenesis is unclear. To address the genetic and cellular origins of this disease, a novel Drosophila GBM model has been developed in which glial progenitor cells give rise to proliferative and invasive neoplastic cells that create transplantable tumors in response to constitutive co-activation of the EGFR-Ras and PI3K pathways. Standing with a rich literature demonstrating the direct relevance of Drosophila to studies on human cancer, neurological disease, and neurodevelopment, this model represents a robust cell-type specific Drosophila neurological disease model in which malignant cells are created by mutations in genetic pathways thought to be driving forces in a homologous human disease. Using lineage analysis and cell-type specific markers, neoplastic glial cells were found to originate from committed glial progenitor cells, rather than from multipotent neuroblasts. Genetic analyses demonstrated that EGFR-Ras and PI3K induce fly glial neoplasia through activation of a combinatorial genetic network composed, in part, of other genetic pathways also commonly mutated in human glioblastomas. In the future, large-scale forward genetic screens with this model may reveal new insights into the origins and treatments of human glioblastoma.
Indexed as
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.