ArticleOncogene2006
Characterization of an imatinib-sensitive subset of high-grade human glioma cultures.
Article in Oncogene, 2006. 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, 99 citations in OpenAlex.
- Multicentre phase II studies evaluating imatinib plus hydroxyurea in patients with progressive glioblastoma.British journal of cancer · 2009Trial
- Phase II study of imatinib in patients with recurrent gliomas of various histologies: a European Organisation for Research and Treatment of Cancer Brain Tumor Group Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2008Trial
- Pericytes in hematogenous metastasis: mechanistic insights and therapeutic approaches.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Improving the Response of High-Grade Glioma (HGG) Cells to Temozolomide Treatment Through Combination With Imatinib.Cureus · 2025Article
- Article
- VEGFR2 blockade inhibits glioblastoma cell proliferation by enhancing mitochondrial biogenesis.Journal of translational medicine · 2024Article
- Small molecule-mediated disruption of ribosome biogenesis synergizes with FGFR inhibitors to suppress glioma cell growth.Neuro-oncology · 2023Article
- Altered cytoskeletal status in the transition from proneural to mesenchymal glioblastoma subtypes.Scientific reports · 2022Article
- SFRP2 induces a mesenchymal subtype transition by suppression of SOX2 in glioblastoma.Oncogene · 2021Article
- High-Resolution Imaging of Tumor Spheroids and Organoids Enabled by Expansion Microscopy.Frontiers in molecular biosciences · 2020Article
- An orthotopic glioblastoma animal model suitable for high-throughput screenings.Neuro-oncology · 2018Article
- Article
- Serglycin as a potential biomarker for glioma: association of serglycin expression, extent of mast cell recruitment and glioblastoma progression.Oncotarget · 2017Article
- Sex-Divergent Clinical Outcomes and Precision Medicine: An Important New Role for Institutional Review Boards and Research Ethics Committees.Frontiers in pharmacology · 2017Review
- Sunitinib Possible Sex-Divergent Therapeutic Outcomes.Clinical drug investigation · 2016Review
- Glioma-derived plasminogen activator inhibitor-1 (PAI-1) regulates the recruitment of LRP1 positive mast cells.Oncotarget · 2015Article
- Targeting the VEGF and PDGF signaling pathway in glioblastoma treatment.International journal of clinical and experimental pathology · 2015Article
- Molecular biology of gliomas: present and future challenges.Translational medicine @ UniSa · 2014Review
- Glioma-derived macrophage migration inhibitory factor (MIF) promotes mast cell recruitment in a STAT5-dependent manner.Molecular oncology · 2014Article
- Sestrin-2, a repressor of PDGFRβ signalling, promotes cigarette-smoke-induced pulmonary emphysema in mice and is upregulated in individuals with COPD.Disease models & mechanisms · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
High-grade gliomas, including glioblastomas, are malignant brain tumors for which improved treatment is urgently needed. Genetic studies have demonstrated the existence of biologically distinct subsets. Preliminary studies have indicated that platelet-derived growth factor (PDGF) receptor signaling contributes to the growth of some of these tumors. In this study, human high-grade glioma primary cultures were analysed for sensitivity to treatment with the PDGF receptor inhibitor imatinib/Glivec/Gleevec/STI571. Six out of 15 cultures displayed more than 40% growth inhibition after imatinib treatment, whereas seven cultures showed less than 20% growth inhibition. In the sensitive cultures, apoptosis contributed to growth inhibition. Platelet-derived growth factor receptor status correlated with imatinib sensitivity. Supervised analyses of gene expression profiles and real-time PCR analyses identified expression of the chemokine CXCL12/SDF-1 (stromal cell-derived factor 1) as a predictor of imatinib sensitivity. Exogenous addition of CXCL12 to imatinib-insensitive cultures conferred some imatinib sensitivity. Finally, coregulation of CXCL12 and PDGF alpha-receptor was observed in glioblastoma biopsies. We have thus defined the characteristics of a novel imatinib-sensitive subset of glioma cultures, and provided evidence for a functional relationship between imatinib sensitivity and chemokine signaling. These findings will assist in the design and evaluation of clinical trials exploring therapeutic effects of imatinib on malignant brain tumors.
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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.