HealthValue
Fields of HGF/c-Met involvement
HGF/c-Met and cancer
Cancer therapies addressing HGF/c-Met
HGF/c-Met and cancer
HGF
c-Met
c-Met
Ras
Grb2
Raf
Mek
MAPK
Gab1
PI3K
STAT3
b Catenin
activation
Increased
protease
production
Cell dissociation :
metastasis
Endothelial cell
proliferation
Neoangiogenesis
c-Met activation by HGF has 3 consequences in cancer :

- Endothelial cell proliferation

- Activation of key oncogenic pathways :
  the Ras pathway,
  the PI3K/STAT3 pathway,           the b Catenin pathway

- Increased protease production and hence cell dissociation leading to metastasis
Abbreviations : ERK extracellular regulated kinase, Gab1 growth factor receptor bound protein 2 associated binder 1, GRB2 growth factor receptor bound protein 2, HGF hepatocyte growth factor, MAPK mitogen activated protein kinase, Mek MAP-ERK kinase, PI3K phosphoinositide kinase, STAT signal transducer and activator of transcription, Raf rat fibrosarcoma, Ras rat sarcoma
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Cells/organelles
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cells
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exons
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lysosomes
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ABOUT MONOCLONALS
what is a monoclonal
chains & fragments
therapeutic fields
what are CDs
types of monoclonals
fusion proteins
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making monoclonals
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MET
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Ras
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MONOCLONALS
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Her3
In gefitinib/erlotinib resistant cells
c-Met can phosphorylate Her3,
leading to activation of the PI3K pathway. This constitutes an
escape route for cancer cells