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Updated: Jun 5, 2026
Implantation and Monitoring by PET/CT of an Orthotopic Model of Human Pleural Mesothelioma in Athymic Mice
Published on: December 21, 2019
Antiangiogenic therapies for malignant pleural mesothelioma
1Division of Medical Oncology, Cancer Research Institute, Kanazawa University. Kanazawa, Ishikawa 920-0934, Japan. syano@staff.kanazawa-u.ac.jp
Abstract:
Malignant pleural mesothelioma (MPM), arises from the mesothelial cells, is difficult to be diagnosed at an early stage, and is refractory to conventional chemotherapy and radiotherapy. Therefore, the establishment of novel effective therapies is necessary to improve the prognosis for many patients with this disease. Recent studies have demonstrated that angiogenesis plays a significant role in MPM progression, suggesting the importance of tumor vessels as therapeutic targets. To explore molecular pathogenesis and evaluate the efficacy of vascular targeting therapy in MPM, we developed orthotopic implantation SCID mouse models of MPM. We found that selective VEGF inhibitors were effective only in the treatment of high-VEGF-producing MPM models. On the other hand, multiple kinase inhibitor E7080, with inhibitory activity against various angiogenic cytokine receptors, suppressed the progression and prolonged survival of both high-VEGF-producing and low-VEGF-producing MPM models. Further understanding of the functional characteristics of tumor angiogenesis may be essential to improve targeting therapies in MPM. In this review, we introduce current status of clinical strategies and novel therapeutic approaches against angiogenesis in MPM.
Insights
Malignant pleural mesothelioma (MPM) requires new therapies. A multi-kinase inhibitor, E7080, effectively targeted tumor angiogenesis and improved survival in MPM mouse models, unlike VEGF inhibitors alone.
Area of Science:
- Oncology
- Vascular Biology
- Mesothelioma Research
Background:
- Malignant pleural mesothelioma (MPM) is challenging to diagnose early and resistant to standard treatments.
- Tumor angiogenesis is a critical factor in MPM progression, making tumor vasculature a potential therapeutic target.
Purpose of the Study:
- To investigate the molecular pathogenesis of MPM.
- To evaluate the efficacy of vascular targeting therapies in MPM using orthotopic SCID mouse models.
Main Methods:
- Development of orthotopic implantation SCID mouse models of MPM.
- Assessment of selective VEGF inhibitors and the multi-kinase inhibitor E7080 in MPM models.
- Evaluation of tumor progression and survival rates.
Main Results:
- Selective VEGF inhibitors showed efficacy only in high-VEGF-producing MPM models.
- The multi-kinase inhibitor E7080 suppressed progression and prolonged survival in both high- and low-VEGF-producing MPM models.
- E7080 demonstrated broader efficacy by inhibiting multiple angiogenic cytokine receptors.
Conclusions:
- Targeting tumor angiogenesis is a promising strategy for MPM treatment.
- Multi-kinase inhibitors like E7080 offer a potential therapeutic advantage over selective VEGF inhibitors for MPM.
- Further research into tumor angiogenesis mechanisms is crucial for advancing MPM therapies.
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