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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
Published on: September 30, 2016
The hepatocyte growth factor/c-Met signaling pathway as a therapeutic target to inhibit angiogenesis
Weon-Kyoo You1, Donald M McDonald
1Department of Anatomy, University of California, San Francisco, California, USA. weon-kyoo.you@ucsf.edu
Abstract:
Angiogenesis in tumors is driven by multiple growth factors that activate receptor tyrosine kinases. An important driving force of angiogenesis in solid tumors is signaling through vascular endothelial growth factor (VEGF) and its receptors (VEGFRs). Angiogenesis inhibitors that target this signaling pathway are now in widespread use for the treatment of cancer. However, when used alone, inhibitors of VEGF/VEGFR signaling do not destroy all blood vessels in tumors and do not slow the growth of most human cancers. VEGF/VEGFR signaling inhibitors are, therefore, used in combination with chemotherapeutic agents or radiation therapy. Additional targets for inhibiting angiogenesis would be useful for more efficacious treatment of cancer. One promising target is the signaling pathway of hepatocyte growth factor (HGF) and its receptor (HGFR, also known as c-Met), which plays important roles in angiogenesis and tumor growth. Inhibitors of this signaling pathway have been shown to inhibit angiogenesis in multiple in vitro and in vivo models. The HGF/c-Met signaling pathway is now recognized as a promising target in cancer by inhibiting angiogenesis, tumor growth, invasion, and metastasis.
Insights
Targeting the hepatocyte growth factor (HGF)/c-Met pathway offers a new strategy to inhibit tumor angiogenesis and growth. This approach complements existing vascular endothelial growth factor (VEGF) therapies for more effective cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Tumor angiogenesis is crucial for cancer growth, primarily driven by vascular endothelial growth factor (VEGF) signaling.
- Current anti-angiogenesis therapies targeting VEGF/VEGFR show limitations, necessitating combination treatments or novel targets.
- The hepatocyte growth factor (HGF)/c-Met pathway is implicated in tumor angiogenesis and progression.
Purpose of the Study:
- To explore the potential of the HGF/c-Met signaling pathway as a therapeutic target for inhibiting tumor angiogenesis and growth.
- To evaluate the efficacy of HGF/c-Met pathway inhibitors in preclinical cancer models.
Main Methods:
- Review of existing literature on angiogenesis, VEGF/VEGFR, and HGF/c-Met signaling pathways.
- Analysis of in vitro and in vivo studies investigating HGF/c-Met inhibitors' effects on angiogenesis and tumor growth.
Main Results:
- HGF/c-Met signaling plays a significant role in tumor angiogenesis and growth.
- Inhibitors of the HGF/c-Met pathway have demonstrated efficacy in reducing angiogenesis in various experimental models.
- The HGF/c-Met pathway is recognized as a promising target for cancer therapy.
Conclusions:
- Targeting the HGF/c-Met pathway presents a viable strategy to enhance anti-cancer therapies.
- Inhibiting HGF/c-Met signaling can impede tumor angiogenesis, growth, invasion, and metastasis.
- Further research into HGF/c-Met inhibitors could lead to improved cancer treatment outcomes.
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