Targeting MET in cancer therapy
MET encodes a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF). The specific combination of c-MET and HGF activates downstream signaling pathways to trigger cell migration, proliferation, and angiogenesis. MET exon 14 alterations and MET gene amplification play a critical role in th...
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KeAi Communications Co., Ltd.
2017
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oai:doaj.org-article:de222e61f8fd42a8a74c780b8dd370cb2021-12-02T10:50:32ZTargeting MET in cancer therapy2095-882X10.1016/j.cdtm.2017.06.002https://doaj.org/article/de222e61f8fd42a8a74c780b8dd370cb2017-09-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2095882X16301633https://doaj.org/toc/2095-882XMET encodes a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF). The specific combination of c-MET and HGF activates downstream signaling pathways to trigger cell migration, proliferation, and angiogenesis. MET exon 14 alterations and MET gene amplification play a critical role in the origin of cancer. Several monoclonal antibodies and small-molecule inhibitors of c-MET have been evaluated in clinical trials. In patients with advanced non-small cell lung cancer, cabozantinib and crizotinib showed clear efficacy with a generally tolerable adverse events profile. In gastrointestinal cancers, most phase III trials of MET inhibitors showed negative results. In hepatocellular carcinoma, based on the encouraging results of some phase II studies, a series of phase III trials are currently recruiting patients to access the efficacy and safety of MET inhibitors. Keywords: Proto-oncogene protein c-MET, Antineoplastic agents, Protein kinase inhibitors, Molecular targeted therapyHong-Nan MoPeng LiuKeAi Communications Co., Ltd.articleMedicine (General)R5-920ENChronic Diseases and Translational Medicine, Vol 3, Iss 3, Pp 148-153 (2017) |
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Medicine (General) R5-920 |
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Medicine (General) R5-920 Hong-Nan Mo Peng Liu Targeting MET in cancer therapy |
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MET encodes a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF). The specific combination of c-MET and HGF activates downstream signaling pathways to trigger cell migration, proliferation, and angiogenesis. MET exon 14 alterations and MET gene amplification play a critical role in the origin of cancer. Several monoclonal antibodies and small-molecule inhibitors of c-MET have been evaluated in clinical trials. In patients with advanced non-small cell lung cancer, cabozantinib and crizotinib showed clear efficacy with a generally tolerable adverse events profile. In gastrointestinal cancers, most phase III trials of MET inhibitors showed negative results. In hepatocellular carcinoma, based on the encouraging results of some phase II studies, a series of phase III trials are currently recruiting patients to access the efficacy and safety of MET inhibitors. Keywords: Proto-oncogene protein c-MET, Antineoplastic agents, Protein kinase inhibitors, Molecular targeted therapy |
format |
article |
author |
Hong-Nan Mo Peng Liu |
author_facet |
Hong-Nan Mo Peng Liu |
author_sort |
Hong-Nan Mo |
title |
Targeting MET in cancer therapy |
title_short |
Targeting MET in cancer therapy |
title_full |
Targeting MET in cancer therapy |
title_fullStr |
Targeting MET in cancer therapy |
title_full_unstemmed |
Targeting MET in cancer therapy |
title_sort |
targeting met in cancer therapy |
publisher |
KeAi Communications Co., Ltd. |
publishDate |
2017 |
url |
https://doaj.org/article/de222e61f8fd42a8a74c780b8dd370cb |
work_keys_str_mv |
AT hongnanmo targetingmetincancertherapy AT pengliu targetingmetincancertherapy |
_version_ |
1718396620378210304 |