ArticleMolecular cancer therapeutics2015
Radiosensitization of Primary Human Glioblastoma Stem-like Cells with Low-Dose AKT Inhibition.
Article in Molecular cancer therapeutics, 2015. 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.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Exploring the role of 4D printing materials, techniques, and characteristics for personalized oncology.Translational oncology · 2026Review
- Aldo-keto reductase family 1 member C3 mediates radioresistance of esophageal cancer cells through suppressing MAPK and AKT signaling.BMC cancer · 2024Article
- A Sequential Targeting Strategy Interrupts AKT-Driven Subclone-Mediated Progression in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Current Research Trends in the Application of In Vitro Three-Dimensional Models of Liver Cells.Pharmaceutics · 2022Review
- Bone morphogenetic protein receptor inhibitors suppress the growth of glioblastoma cells.Molecular and cellular biochemistry · 2022Article
- Small Molecule Inhibitors in Adult High-Grade Glioma: From the Past to the Future.Frontiers in oncology · 2022Review
- Article
- Generation of glioblastoma patient-derived organoids and mouse brain orthotopic xenografts for drug screening.STAR protocols · 2021Article
- The multi-target small-molecule inhibitor SB747651A shows in vitro and in vivo anticancer efficacy in glioblastomas.Scientific reports · 2021Article
- Review
- Rapid Processing and Drug Evaluation in Glioblastoma Patient-Derived Organoid Models with 4D Bioprinted Arrays.iScience · 2020Article
- Teaching an Old Drug New Tricks: Dexamethasone as an In Vivo Inhibitor of Glioblastoma Dispersal.Cureus · 2020Article
- Differential effects of the Akt inhibitor MK-2206 on migration and radiation sensitivity of glioblastoma cells.BMC cancer · 2019Article
- Radioresistance of cancer cells, integrin αvβ3 and thyroid hormone.Oncotarget · 2018Review
- Magnetic hyperthermia therapy for the treatment of glioblastoma: a review of the therapy's history, efficacy and application in humans.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2018Review
- Coherent Timescales and Mechanical Structure of Multicellular Aggregates.Biophysical journal · 2018Article
- Dexamethasone-Mediated Upregulation of Calreticulin Inhibits Primary Human Glioblastoma Dispersal Ex Vivo.International journal of molecular sciences · 2018Article
- Delta-6-desaturase inhibitor enhances radiation therapy in glioblastoma in vitro and in vivo.Cancer management and research · 2018Article
- Utility of Glioblastoma Patient-Derived Orthotopic Xenografts in Drug Discovery and Personalized Therapy.Frontiers in oncology · 2018Article
- A molecular view of the radioresistance of gliomas.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most frequent and lethal brain cancer. The lack of early detection methods, the presence of rapidly growing tumor cells, and the high levels of recurrence due to chemo- and radioresistance make this cancer an extremely difficult disease to treat. Emerging studies have focused on inhibiting AKT activation; here, we demonstrate that in primary GBM tumor samples, full-dose inhibition of AKT activity leads to differential responses among samples in the context of cell death and self-renewal, reinforcing the notion that GBM is a heterogeneous disease. In contrast, low-dose AKT inhibition when combined with fractionation of radiation doses leads to a significant apoptosis-mediated cell death of primary patient-derived GBM cells. Therefore, low-dose-targeted therapies might be better for radiosensitization of primary GBM cells and further allow for reducing the clinical toxicities often associated with targeting the AKT/PI3K/mTOR pathway. This work emphasizes the discrepancies between cell lines and primary tumors in drug testing, and indicates that there are salient differences between patients, highlighting the need for personalized medicine in treating high-grade glioma.
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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.