Abstract:
:The c-Met/hepatocyte growth factor receptor and its family members are known to promote cancer cell migration and invasion. Signaling within and beyond this pathway contributes to the systemic spread of metastases through induction of the epithelial-mesenchymal transition, a process also implicated in mediating resistance to current anticancer therapies, including radiation. Induction of c-Met has also been observed after irradiation, suggesting that c-Met participates in radiation-induced disease progression through the epithelial-mesenchymal transition. Therefore, c-Met inhibition is an attractive target for potentially mitigating radiation resistance. This article summarizes key findings regarding crosstalk between radiotherapy and c-Met and discusses studies performed to date in which c-Met inhibition was used as a strategy to increase cellular radiosensitivity.
journal_name
Cancerjournal_title
Cancerauthors
Bhardwaj V,Cascone T,Cortez MA,Amini A,Evans J,Komaki RU,Heymach JV,Welsh JWdoi
10.1002/cncr.27965subject
Has Abstractpub_date
2013-05-15 00:00:00pages
1768-75issue
10eissn
0008-543Xissn
1097-0142journal_volume
119pub_type
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