ArticleBioMed research international2015
Inhibition of PI3K Signalling Selectively Affects Medulloblastoma Cancer Stem Cells.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 32 citations in OpenAlex.
- NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation.Redox biology · 2026Article
- CD133 structural instability as a gateway to medulloblastoma vulnerability.Cancer cell international · 2026Article
- TrkA activation sustains chemotherapy resistance in chemotolerant medulloblastoma cells.Acta neuropathologica communications · 2026Article
- The resilient subset: cancer stem cells at the core of immunotherapy resistance.Immunotherapy advances · 2026Review
- The pivotal role of autophagy in the pathogenesis and therapy of medulloblastoma.Future oncology (London, England) · 2024Review
- PP2A activation overcomes leptomeningeal dissemination in group 3 medulloblastoma.The Journal of biological chemistry · 2024Article
- Overcoming Treatment Resistance in Medulloblastoma: Underlying Mechanisms and Potential Strategies.Cancers · 2024Review
- Molecular and functional profiling of chemotolerant cells unveils nucleoside metabolism-dependent vulnerabilities in medulloblastoma.Acta neuropathologica communications · 2023Article
- Molecular Docking as a Therapeutic Approach for Targeting Cancer Stem Cell Metabolic Processes.Frontiers in pharmacology · 2022Review
- KIF26B Is Overexpressed in Medulloblastoma and Promotes Malignant Progression by Activating the PI3K/AKT Pathway.Analytical cellular pathology (Amsterdam) · 2022Article
- Microfluidic Lab-on-a-Chip Based on UHF-Dielectrophoresis for Stemness Phenotype Characterization and Discrimination among Glioblastoma Cells.Biosensors · 2021Article
- Tumor Growth in the High Frequency Medulloblastoma Mouse Model Ptch1Frontiers in oncology · 2021Article
- Article
- Article
- Pharmacological mTOR targeting enhances the antineoplastic effects of selective PI3Kα inhibition in medulloblastoma.Scientific reports · 2019Article
- Sonic Hedgehog Medulloblastoma Cancer Stem Cells Mirnome and Transcriptome Highlight Novel Functional Networks.International journal of molecular sciences · 2018Article
- Targeting mTOR as a Therapeutic Approach in Medulloblastoma.International journal of molecular sciences · 2018Review
- Stimulation of medulloblastoma stem cells differentiation by a peptidomimetic targeting neuropilin-1.Oncotarget · 2018Article
- FFJ-3 inhibits PKM2 protein expression via the PI3K/Akt signaling pathway and activates the mitochondrial apoptosis signaling pathway in human cancer cells.Oncology letters · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medulloblastoma is the most common malignant brain tumor of childhood. Although survival has slowly increased in the past years, the prognosis of these patients remains unfavourable. In this context, it has been recently shown that the intracellular signaling pathways activated during embryonic cerebellar development are deregulated in MDB. One of the most important is PI3K/AKT/mTOR, implicated in cell proliferation, survival, growth, and protein synthesis. Moreover, a fraction of MDB cells has been shown to posses stemlike features, to express typical neuronal precursor markers (Nestin and CD133), and to be maintained by the hypoxic cerebellar microenvironment. This subpopulation of MDB cells is considered to be responsible for treatment resistance and recurrence. In this study, we evaluated the effects of PI3K/AKT pathway inhibition on primary cultures of MDB and particularly on the cancer stem cell (CSC) population (CD133(+)). PI3K inhibition was able to counteract MDB cell growth and to promote differentiation of stemlike MDB cells. Moreover, PI3K/AKT pathway suppression induced dramatic cell death through activation of the mitochondrial proapoptotic cascade. Finally, analysis on the stem cells fraction revealed that the MDB CSC population is more sensitive to PI3K targeting compared to the whole cancerous population and its nonstem cell counterpart.
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.