ArticleJournal of neuro-oncology2010
In-vitro effects of the tyrosine kinase inhibitor imatinib on glioblastoma cell proliferation.
Article in Journal of neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Phase I-II trial of imatinib mesylate (Gleevec; STI571) in treatment of recurrent oligodendroglioma and mixed oligoastrocytoma. North central cancer treatment group study N0272 (ALLIANCE/NCCTG).Journal of neuro-oncology · 2019Trial
- Role of the TLR signaling pathway in the pathogenesis of glioblastoma multiforme with an emphasis on immunotherapy.Biochemistry and biophysics reports · 2025Review
- Review
- EPHA2 mediates PDGFA activity and functions together with PDGFRA as prognostic marker and therapeutic target in glioblastoma.Signal transduction and targeted therapy · 2022Article
- Molecular Alterations and Their Correlation With the Survival of Glioblastoma Patients With Corpus Callosum Involvement.Frontiers in neuroscience · 2021Article
- Autophagic and Apoptotic Pathways as Targets for Chemotherapy in Glioblastoma.International journal of molecular sciences · 2018Review
- ERBB3, IGF1R, and TGFBR2 expression correlate with PDGFR expression in glioblastoma and participate in PDGFR inhibitor resistance of glioblastoma cells.American journal of cancer research · 2018Article
- Development of targeted therapies in treatment of glioblastoma.Cancer biology & medicine · 2015Review
- Targeting the VEGF and PDGF signaling pathway in glioblastoma treatment.International journal of clinical and experimental pathology · 2015Article
- Article
- Inhibition of receptor signaling and of glioblastoma-derived tumor growth by a novel PDGFRβ aptamer.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- In Vitro and In Vivo Analysis of RTK Inhibitor Efficacy and Identification of Its Novel Targets in Glioblastomas.Translational oncology · 2013Article
- t-AUCB, an improved sEH inhibitor, suppresses human glioblastoma cell growth by activating NF-κB-p65.Journal of neuro-oncology · 2012Article
- Antiangiogenic therapy for glioma.Journal of signal transduction · 2012Article
- Novel therapies in glioblastoma.Neurology research international · 2012Article
- Decreased therapeutic effects of noscapine combined with imatinib mesylate on human glioblastoma in vitro and the effect of midkine.Cancer cell international · 2011Article
- Delivery of molecularly targeted therapy to malignant glioma, a disease of the whole brain.Expert reviews in molecular medicine · 2011Review
- Article
- Three paths to better tyrosine kinase inhibition behind the blood-brain barrier in treating chronic myelogenous leukemia and glioblastoma with imatinib.Translational oncology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBL) is the most malignant brain tumour in adults, causing the death of most patients within 9-12 months of diagnosis. Treatment is based on a combination of surgery, radiation therapy, and chemotherapy. With these treatment modalities, however, responses are extremely poor, so identification of novel treatment strategies is highly warranted. Platelet-derived growth factors (PDGF) and their receptors are commonly coexpressed in GBL, suggesting that stimulation of autocrine PDGF receptors may contribute to their growth. Interest in these receptors as drug target for glioblastoma treatment has increased with the clinical availability of the PDGFR kinase inhibitor antagonist imatinib mesylate (STI571). In this study, T98G and A172 human GBL cell lines were analysed for their sensitivity to treatment with imatinib. In particular, we focussed our attention on analysis of DNA distribution by flow cytometry at different times of incubation with different imatinib concentrations (1-30 microM: ). Our results show that imatinib induces growth arrest in T98G and A172 cells in the G(0)/G(1) phase of the cell cycle, at all the concentrations tested, as early as 24 h after treatment. However we have also seen, by means of annexin V staining, that at 20 and 30 microM: concentrations, in concomitance with a significant growth arrest in the G(0)/G(1) phase, there is an increase of apoptotic cells 48 h after treatment, suggesting that imatinib at low concentrations (1-10 microM: ) could act as a cytostatic agent whereas at high concentrations (20, 30 microM: ) it mainly behaves as a cytotoxic agent.
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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.