ArticleJournal of cellular physiology2015
Sorafenib/regorafenib and lapatinib interact to kill CNS tumor cells.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- GATESynergy: Integrating Molecular Global-Local Aggregator and Hierarchical Gene-Gated Encoder for Drug Synergy Prediction.Interdisciplinary sciences, computational life sciences · 2026Article
- Comprehensive In Silico Investigation of L-Glutamine Transporters and Metabolism in Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Potential Drug Synergy Through the ERBB2 Pathway in HER2+ Breast Tumors.International journal of molecular sciences · 2024Article
- Integrated multiomic analysis reveals disulfidptosis subtypes in glioblastoma: implications for immunotherapy, targeted therapy, and chemotherapy.Frontiers in immunology · 2024Article
- Review
- Targeting hyaluronic acid synthase-3 (HAS3) for the treatment of advanced renal cell carcinoma.Cancer cell international · 2022Article
- Clinical and NGS predictors of response to regorafenib in recurrent glioblastoma.Scientific reports · 2022Article
- Recurrent Glioblastoma Treatment: State of the Art and Future Perspectives in the Precision Medicine Era.Biomedicines · 2022Review
- Small Molecule Inhibitors in Adult High-Grade Glioma: From the Past to the Future.Frontiers in oncology · 2022Review
- Novel Receptor Tyrosine Kinase Pathway Inhibitors for Targeted Radionuclide Therapy of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A molecular signature associated with prolonged survival in glioblastoma patients treated with regorafenib.Neuro-oncology · 2021Article
- Identification of Iron Metabolism-Related Genes as Prognostic Indicators for Lower-Grade Glioma.Frontiers in oncology · 2021Article
- Regorafenib in Glioblastoma Recurrence: How to Deal With MR Imaging Treatments Changes.Frontiers in radiology · 2021Review
- Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Revisiting anti-angiogenic therapy for recurrent glioblastoma.Translational cancer research · 2019Article
- Regorafenib CSF Penetration, Efficacy, and MRI Patterns in Recurrent Malignant Glioma Patients.Journal of clinical medicine · 2019Article
- Inhibition of Autophagy by Chloroquine Enhances the Antitumor Efficacy of Sorafenib in Glioblastoma.Cellular and molecular neurobiology · 2016Article
- Sorafenib inhibits cell growth but fails to enhance radio- and chemosensitivity of glioblastoma cell lines.Oncotarget · 2016Article
- Ruxolitinib synergizes with DMF to kill via BIM+BAD-induced mitochondrial dysfunction and via reduced SOD2/TRX expression and ROS.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The present studies were to determine whether the multi-kinase inhibitor sorafenib or its derivative regorafenib interacted with the ERBB1/ERBB2 inhibitor lapatinib to kill CNS tumor cells. In multiple CNS tumor cell types sorafenib and lapatinib interacted in a greater than additive fashion to cause tumor cell death. Tumor cells lacking PTEN, and anoikis or lapatinib resistant cells were as sensitive to the drug combination as cells expressing PTEN or parental cells, respectively. Similar data were obtained using regorafenib. Treatment of brain cancer cells with [sorafenib + lapatinib] enhanced radiation toxicity. The drug combination increased the numbers of LC3-GFP vesicles; this correlated with a reduction in endogenous LC3II, and p62 and LAMP2 degradation. Knock down of Beclin1 or ATG5 significantly suppressed drug combination lethality. Expression of c-FLIP-s, BCL-XL, or dominant negative caspase 9 reduced drug combination toxicity; knock down of FADD or CD95 was protective. Expression of both activated AKT and activated MEK1 or activated mTOR was required to strongly suppress drug combination lethality. As both lapatinib and sorafenib are FDA approved agents, our data argue for further determination as to whether lapatinib and sorafenib is a useful glioblastoma therapy.
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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.