ArticleNeoplasia (New York, N.Y.)2005
mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma.
Article in Neoplasia (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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
95 citing papers in PubMed, 197 citations in OpenAlex.
- A pilot study of everolimus and gefitinib in the treatment of recurrent glioblastoma (GBM).Journal of neuro-oncology · 2009Trial
- Pericytes orchestrate a tumor-restraining microenvironment in glioblastoma.Nature communications · 2025Article
- In vivo mouse models for adult brain tumors: Exploring tumorigenesis and advancing immunotherapy development.Neuro-oncology · 2024Review
- Coordinated Targeting of S6K1/2 and AXL Disrupts Pyrimidine Biosynthesis in PTEN-Deficient Glioblastoma.Cancer research communications · 2024Article
- The Oncogenesis of Glial Cells in Diffuse Gliomas and Clinical Opportunities.Neuroscience bulletin · 2023Review
- Developing Novel Experimental Models of m-TORopathic Epilepsy and Related Neuropathologies: Translational Insights from Zebrafish.International journal of molecular sciences · 2023Review
- Exosomal circRNA BTG2 derived from RBP-J overexpressed-macrophages inhibits glioma progression via miR-25-3p/PTEN.Cell death & disease · 2022Article
- Spreading of Alpha Synuclein from Glioblastoma Cells towards Astrocytes Correlates with Stem-like Properties.Cancers · 2022Article
- Computational modelling of perivascular-niche dynamics for the optimization of treatment schedules for glioblastoma.Nature biomedical engineering · 2021Article
- Review
- Review
- Overcoming the Blood-Brain Barrier: Successes and Challenges in Developing Nanoparticle-Mediated Drug Delivery Systems for the Treatment of Brain Tumours.International journal of nanomedicine · 2020Review
- ABC Transporters at the Blood-Brain Interfaces, Their Study Models, and Drug Delivery Implications in Gliomas.Pharmaceutics · 2019Review
- The Autophagy Status of Cancer Stem Cells in Gliobastoma Multiforme: From Cancer Promotion to Therapeutic Strategies.International journal of molecular sciences · 2019Review
- Arming oHSV with ULBP3 drives abscopal immunity in lymphocyte-depleted glioblastoma.JCI insight · 2019Article
- PIP4K2A as a negative regulator of PI3K in PTENThe Journal of experimental medicine · 2019Article
- Voxel-wise radiogenomic mapping of tumor location with key molecular alterations in patients with glioma.Neuro-oncology · 2018Article
- Identification of expression quantitative trait loci ofOncology letters · 2018Article
- Article
- Antiglioma effects of cytarabine on leptomeningeal metastasis of high-grade glioma by targeting the PI3K/Akt/mTOR pathway.Drug design, development and therapy · 2017Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Combined activation of Ras and AKT leads to the formation of astrocytic glioblastoma multiforme (GBM) in mice. In human GBMs, AKT is not mutated but is activated in approximately 70% of these tumors, in association with loss of PTEN and/or activation of receptor tyrosine kinases. Mechanistic justification for the therapeutic blockade of targets downstream of AKT, such as mTOR, in these cancers requires demonstration that the oncogenic effect of PTEN loss is through elevated AKT activity. We demonstrate here that loss of Pten is similar to AKT activation in the context of glioma formation in mice. We further delineate the role of mTOR activity downstream of AKT in the maintenance of AKT+KRas-induced GBMs. Blockade of mTOR results in regional apoptosis in these tumors and conversion in the character of surviving tumor cells from astrocytoma to oligodendroglioma. These data suggest that mTOR activity is required for the survival of some cells within these GBMs, and mTOR appears required for the maintenance of astrocytic character in the surviving cells. Furthermore, our study provides the first example of conversion between two distinct tumor types usually thought of as belonging to specific lineages, and provides evidence for signal transduction-mediated transdifferentiation between glioma subtypes.
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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.