Study Results from Tsukuba Research Center Update Understanding of Lung Cancer (Triple Inhibition of EGFR, Met, and VEGF Suppresses Regrowth of HGF-Triggered, Erlotinib-Resistant Lung Cancer Harboring an EGFR Mutation)
By a News Reporter-Staff News Editor at Biotech Week -- Research findings on Oncology are discussed in a new report. According to news originating from Ibaraki, Japan, by NewsRx correspondents, research stated, "Met activation by gene amplification and its ligand, hepatocyte growth factor (HGF), imparts resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR-mutant lung cancer. We recently reported that Met activation by HGF stimulates the production of vascular endothelial growth factor (VEGF) and facilitates angiogenesis, which indicates that HGF induces EGFR-TKI resistance and angiogenesis."
Our news journalists obtained a quote from the research from Tsukuba Research Center, "This study aimed to determine the effect of triple inhibition of EGFR, Met, and angiogenesis on HGF-triggered EGFR-TKI resistance in EGFR-mutant lung cancer. Three clinically approved drugs, erlotinib (an EGFR inhibitor), crizotinib (an inhibitor of anaplastic lymphoma kinase and Met), and bevacizumab (anti-VEGF antibody), and TAS-115, a novel dual TKI for Met and VEGF receptor 2, were used in this study. EGFR-mutant lung cancer cell lines PC-9, HCC827, and HGF-gene-transfected PC-9 (PC-9/HGF) cells were examined. Crizotinib and TAS-115 inhibited Met phosphorylation and reversed erlotinib resistance and VEGF production triggered by HGF in PC-9 and HCC827 cells in vitro. Bevacizumab and TAS-115 inhibited angiogenesis in PC-9/HGF tumors in vivo. Moreover, the triplet erlotinib, crizotinib, and bevacizumab, or the doublet erlotinib and TAS-115 successfully inhibited PC-9/HGF tumor growth and delayed tumor regrowth associated with sustained tumor vasculature inhibition even after cessation of the treatment."
According to the news editors, the research concluded: "These results suggest that triple inhibition of EGFR, HGF/Met, and VEGF/VEGF receptor 2, by either a triplet of clinical drugs or TAS-115 combined with erlotinib, may be useful for controlling progression of EGFR-mutant lung cancer by reversing EGFR-TKI resistance and for inhibiting angiogenesis."
For more information on this research see: Triple Inhibition of EGFR, Met, and VEGF Suppresses Regrowth of HGF-Triggered, Erlotinib-Resistant Lung Cancer Harboring an EGFR Mutation. Journal of Thoracic Oncology, 2014;9(6):775-783. Journal of Thoracic Oncology can be contacted at: Lippincott Williams & Wilkins, 530 Walnut St, Philadelphia, PA 19106-3621, USA. (Lippincott Williams and Wilkins - www.lww.com; Journal of Thoracic Oncology - journals.lww.com/jto/pages/default.aspx)
The news correspondents report that additional information may be obtained from J. Nakade, Taiho Pharmaceut Co Ltd, Tsukuba Res Center, Tsukuba, Ibaraki, Japan. Additional authors for this research include S. Takeuchi, T. Nakagawa, D. Ishikawa, T. Sano, S. Nanjo, T. Yamada, H. Ebi, L. Zhao, K. Yasumoto, K. Matsumoto, K. Yonekura and S. Yano (see also Oncology).
Keywords for this news article include: Asia, Antineoplastic Monoclonal Antibodies, Japan, Drugs, Ibaraki, Therapy, Oncology, Erlotinib, Bevacizumab, Lung Cancer, Angiogenesis, Lung Neoplasms, Membrane Proteins, Angiogenic Proteins, Phosphotransferases, Enzymes and Coenzymes, VEGF - VEGFR Inhibitors, Protein Kinase Inhibitors, Tyrosine Kinase Inhibitors
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