ArticleNeuro-oncology2010
Akt signaling pathway: a target for radiosensitizing human malignant glioma.
Article in Neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 71 citations in OpenAlex.
- eIF6 affects the occurrence and development of esophageal cancer.Molecular biology reports · 2026Article
- Synergistic antitumor and radiosensitizing effects of α-sulfoquinovosyl-acylpropanediol (SQAP) via PI3K/Akt inhibition and DNA repair impairment in glioblastoma.Journal of neuro-oncology · 2025Article
- Article
- Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Review
- Prediction of regulatory targets of alternative isoforms of the epidermal growth factor receptor in a glioblastoma cell line.BMC bioinformatics · 2019Article
- Differential effects of the Akt inhibitor MK-2206 on migration and radiation sensitivity of glioblastoma cells.BMC cancer · 2019Article
- Peroxisome Proliferator Activated Receptor Gamma Sensitizes Non-small Cell Lung Carcinoma to Gamma Irradiation Induced Apoptosis.Frontiers in genetics · 2019Article
- PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway.Journal of cellular and molecular medicine · 2018Article
- Natural products: a hope for glioblastoma patients.Oncotarget · 2018Review
- Akt inhibition improves long-term tumour control following radiotherapy by altering the microenvironment.EMBO molecular medicine · 2017Article
- A molecular view of the radioresistance of gliomas.Oncotarget · 2017Review
- Role of STAT3 in Genesis and Progression of Human Malignant Gliomas.Molecular neurobiology · 2017Review
- Combinatorial therapy with adenoviral-mediated PTEN and a PI3K inhibitor suppresses malignant glioma cell growth in vitro and in vivo by regulating the PI3K/AKT signaling pathway.Journal of cancer research and clinical oncology · 2017Article
- Predictive biomarkers of resistance to hypofractionated radiotherapy in high grade glioma.Radiation oncology (London, England) · 2017Article
- Potential therapeutic targets of Guggulsterone in cancer.Nutrition & metabolism · 2017Review
- KIAA0247 suppresses the proliferation, angiogenesis and promote apoptosis of human glioma through inactivation of the AKT and Stat3 signaling pathway.Oncotarget · 2016Article
- Fragile X mental retardation protein promotes astrocytoma proliferation via the MEK/ERK signaling pathway.Oncotarget · 2016Article
- STAT3 Serine 727 Phosphorylation: A Relevant Target to Radiosensitize Human Glioblastoma.Brain pathology (Zurich, Switzerland) · 2016Article
- Therapeutic Implications for Overcoming Radiation Resistance in Cancer Therapy.International journal of molecular sciences · 2015Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation therapy plays a central role in the treatment of glioblastoma, but it is not curative due to the high tumor radioresistance. Phosphatidyl-inositol 3-kinase/protein kinase B (Akt) and Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathways serve to block the apoptosis process, keeping cells alive in very toxic environments such as chemotherapy or ionizing radiation. In the present study, from a panel of 8 human malignant glioma cell lines, investigations on the relationship between intrinsic radioresistance and Akt or STAT3 basal activation were done. Secondly, the impact of down-modulation of Akt or STAT3 signaling on in vitro intrinsic radiosensitivity was evaluated. Using a clonogenic cell survival assay, our results revealed a significant correlation between the basal Akt activation and the surviving fraction at 2 Gy (SF2). In contrast, no correlation was found between STAT3 activation and SF2. According to this, down-modulation of Akt with a specific chemical inhibitor (Akt inhibitor IV) demonstrated a significant enhancement of radiation sensitivity on glioma cells in a clonogenic survival assay. On the contrary, down-modulation of STAT3 signaling with a specific chemical inhibitor (JSI-124) or a neutralizing gp130 antibody failed to radiosensitize glioma cells. These data indicate that the Akt intercept node could be a more relevant therapeutic target than STAT3 for radiosensitizing human malignant 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.