Journal
JOURNAL OF HEMATOLOGY & ONCOLOGY
Volume 9, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s13045-016-0366-y
Keywords
HGF; MET; Lymphoma; Inhibitor
Categories
Funding
- DOD Career Development Award [CA140437]
- SOM Research Enhancement Funding
- Leukemia Research Foundation
- National Natural Science Foundation of China [81272191, 81472547, 81672924, 81400164]
- CDMRP [793839, CA140437] Funding Source: Federal RePORTER
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Inappropriate activation of c-mesenchymal-epithelial transition (MET), the receptor tyrosine kinase (RTK) for hepatocyte growth factor (HGF), has been implicated in tumorigenesis and represented a promising therapeutic target for developing anticancer agents. In contrast to other solid tumors, there are limited data describing the functional role of HGF/c-MET signaling pathway in lymphoma. In the current review, we summarize recent findings about the expression, cellular mechanisms/functions, and therapeutic application of HGF/c-MET in different types of lymphoma, especially B cell lymphoma, T and NK cell lymphoma, and Hodgkin lymphoma. We also discuss the existing problems and future directions about studying the HGF/c-MET pathway in lymphoma cells.
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