ReviewMolecular cancer2017
Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development.
Review in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 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.
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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
159 citing papers in PubMed, 246 citations in OpenAlex.
- Pathway dysregulation and therapeutic resistance in glioblastoma: molecular mechanisms and emerging therapeutic targets.Future science OA · 2026Review
- Corrigendum to: Cellular and in vivo activity of a novel PI3K inhibitor, PX-866, against human glioblastoma.Neuro-oncology · 2026Article
- Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026Review
- Peptides from the Shadows: Molecular Depth Insights and Clinical Horizons of Circular RNA-encoded Peptides in Gliomas.Neuromolecular medicine · 2026Review
- Potential Association of BRAF and PIK3CA Copy Number Alterations with Long-Term Survival in IDH-Wildtype Glioblastoma: A Pilot Study.International journal of molecular sciences · 2026Article
- Review
- Defined pulsed electro-magnetic field exposure suppresses stemness and potentiates temozolomide-induced apoptosis in glioblastoma cells.Scientific reports · 2026Article
- Review
- Triptonide Suppresses AML via PI3K/AKT Signaling: A Network Pharmacology Approach Validated by Molecular Docking and Experimental Studies.Current issues in molecular biology · 2026Article
- Multiple patient-derived glioblastoma models reveal synthetic lethality through concurrent PI3K and CDK4/6 inhibition by blocking trans-active cooperation.Neuro-oncology · 2026Article
- Directed evolution of chlorotoxin enhances MMP-2 recognition and improves CAR-T-cell activity in glioblastoma modelsFrontiers in bioengineering and biotechnology · 2026Article
- Development of a fully human glioblastoma-in-brain-spheroid model for accelerated translational research.Journal of advanced research · 2026Article
- Pathophysiological and Etiological Corroborations for the Mechanistic Design of Intranasal Therapies in Glioblastoma Multiforme.Current pharmaceutical design · 2026Review
- Homologous tumor cell exosome-based drug delivery system co-delivering temozolomide and resveratrol for orthotopic glioblastoma therapy.Pharmaceutical science advances · 2025Article
- Molecular Biomarkers of Glioma.Biomedicines · 2025Review
- Review
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
- New job for an old tool: PI3Kβ phosphorylates OGT to regulate acetyl-CoA in glioblastoma.Trends in cell biology · 2025Article
- InfoScan: A New Transcript Identification Tool Based on scRNA-Seq and Its Application in Glioblastoma.International journal of molecular sciences · 2025Article
- Multidimensional, integrative profiling identifies BCL2L1 methylation as a predictor of MCL1 dependency in pediatric malignancies.JCI insight · 2025Article
99 more citing papers are in PubMed but not listed here.
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 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common and aggressive malignant primary tumor in the central nervous system. One of the most widely used chemotherapeutic drugs for GBM is temozolomide, which is a DNA-alkylating agent and its efficacy is dependent on MGMT methylation status. Little progress in improving the prognosis of GBM patients has been made in the past ten years, urging the development of more effective molecular targeted therapies. Hyper-activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is frequently found in a variety of cancers including GBM, and it plays a central role in the regulation of tumor cell survival, growth, motility, angiogenesis and metabolism. Numerous PI3K inhibitors including pan-PI3K, isoform-selective and dual PI3K/mammalian target of rapamycin (mTOR) inhibitors have exhibited favorable preclinical results and entered clinical trials in a range of hematologic malignancies and solid tumors. Furthermore, combination of inhibitors targeting PI3K and other related pathways may exert synergism on suppressing tumor growth and improving patients' prognosis. Currently, only a handful of PI3K inhibitors are in phase I/II clinical trials for GBM treatment. In this review, we focus on the importance of PI3K/Akt pathway in GBM, and summarize the current development of PI3K inhibitors alone or in combination with other inhibitors for GBM treatment from preclinical to clinical studies.
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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.