ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2014
Efficacy of rapamycin against glioblastoma cancer stem cells.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Therapeutic profiling of dihydroartemisinin using in vitro and in vivo models reveals anti-glioma potential.Cancer cell international · 2026Article
- Glioblastoma at the crossroads: current understanding and future therapeutic horizons.Signal transduction and targeted therapy · 2025Review
- Targeted therapy of cancer stem cells: inhibition of mTOR in pre-clinical and clinical research.Cell death & disease · 2024Review
- Molecular Pathways and Genomic Landscape of Glioblastoma Stem Cells: Opportunities for Targeted Therapy.Cancers · 2022Review
- Article
- Anticancer effects of ABTL0812, a clinical stage drug inducer of autophagy-mediated cancer cell death, in glioblastoma models.Frontiers in oncology · 2022Article
- A Combined Effect of G-Quadruplex and Neuro-Inducers as an Alternative Approach to Human Glioblastoma Therapy.Frontiers in oncology · 2022Article
- Multiple Antitumor Molecular Mechanisms Are Activated by a Fully Synthetic and Stabilized Pharmaceutical Product Delivering the Active Compound Sulforaphane (SFX-01) in Preclinical Model of Human Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Article
- A Systematic Review of Glioblastoma-Targeted Therapies in Phases II, III, IV Clinical Trials.Cancers · 2021Review
- Deciphering the Role of Autophagy in Treatment of Resistance Mechanisms in Glioblastoma.International journal of molecular sciences · 2021Review
- mTOR Modulates Intercellular Signals for Enlargement and Infiltration in Glioblastoma Multiforme.Cancers · 2020Review
- Induction of Lysosome Membrane Permeabilization as a Therapeutic Strategy to Target Pancreatic Cancer Stem Cells.Cancers · 2020Article
- The Botanical Drug PBI-05204, a Supercritical COFrontiers in pharmacology · 2020Article
- Article
- Tivantinib Hampers the Proliferation of Glioblastoma Cells via PI3K/Akt/Mammalian Target of Rapamycin (mTOR) Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The Autophagy Status of Cancer Stem Cells in Gliobastoma Multiforme: From Cancer Promotion to Therapeutic Strategies.International journal of molecular sciences · 2019Review
- Article
- The first-in-class alkylating deacetylase inhibitor molecule tinostamustine shows antitumor effects and is synergistic with radiotherapy in preclinical models of glioblastoma.Journal of hematology & oncology · 2018Article
- A fully coupled space-time multiscale modeling framework for predicting tumor growth.Computer methods in applied mechanics and engineering · 2017Article
- Rapamycin promotes differentiation increasing βIII-tubulin, NeuN, and NeuroD while suppressing nestin expression in glioblastoma cells.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe cancer stem cell (CSC) hypothesis suggests a hierarchical organization of cells within the tumor, in which only a subpopulation of stem-like cells is responsible for the rise and progression of the tumor. Glioblastomas (GBM), a lethal brain tumor, may contain a variable proportion of active CSCs. On the other hand, the phosphatidylinositol 3-kinase (PI3 K)/Akt/mammalian target of rapamycin (mTOR) pathway is highly active in up to 70 % of GBM. The kinase mTOR is a key component of the PI3K pathway that mediates the regulation of growth and cell survival signaling. However, clinical trials with rapamycin, an effective inhibitor of mTOR, have not been up to the created expectations and a plausible explanation is missing. In this work, we analyze the effect of rapamycin on the GBM-CSC population.
methodsThe efficacy of rapamycin in vitro was tested on two primary cell lines derived from human GBM surgical resections that fulfill the criteria to be considered as CSCs. We confirmed the inhibition state of the PI3K/Akt/mTOR pathway analyzing the mTOR direct target ribosomal protein S6. We assayed the growth rate, CD133 expression and ability of forming colonies in soft agar of the CSCs under different doses of rapamycin. The efficacy of rapamycin in vivo was assayed in a CSCs-based orthotopic xenograft. RESULTS AND
conclusionsWe report the efficacy of rapamycin by reducing CSCs proliferation and tumorigenic potential in vitro. Despite these encouraging results, the efficacy in vivo was very poor. This finding confirms the limited use of rapamycin as a monotherapy for glioblastomas.
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.