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2015 ; 7
(Suppl 1
): 13-31
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c-Met as a Target for Personalized Therapy
#MMPMID26628860
Garajová I
; Giovannetti E
; Biasco G
; Peters GJ
Transl Oncogenomics
2015[]; 7
(Suppl 1
): 13-31
PMID26628860
show ga
MET and its ligand HGF are involved in many biological processes, both
physiological and pathological, making this signaling pathway an attractive
therapeutic target in oncology. Downstream signaling effects are transmitted via
mitogen-activated protein kinase (MAPK), PI3K (phosphoinositide 3-kinase protein
kinase B)/AKT, signal transducer and activator of transcription proteins (STAT),
and nuclear factor-?B. The final output of the terminal effector components of
these pathways is activation of cytoplasmic and nuclear processes leading to
increases in cell proliferation, survival, mobilization and invasive capacity. In
addition to its role as an oncogenic driver, increasing evidence implicates MET
as a common mechanism of resistance to targeted therapies including EGFR and
VEGFR inhibitors. In the present review, we summarize the current knowledge on
the role of the HGF-MET signaling pathway in cancer and its therapeutic targeting
(HGF activation inhibitors, HGF inhibitors, MET antagonists and
selective/nonselective MET kinase inhibitors). Recent advances in understanding
the role of this pathway in the resistance to current anticancer strategies used
in lung, kidney and pancreatic cancer are discussed.
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