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Literature summary for 2.7.10.1 extracted from

  • Kentsis, A.; Reed, C.; Rice, K.; Sanda, T.; Rodig, S.; Tholouli, E.; Christie, A.; Valk, P.; Delwel, R.; Ngo, V.; Kutok, J.; Dahlberg, S.; Moreau, L.; Byers, R.; Christensen, J.; Woude, G.; Licht, J.; Kung, A.; Staudt, L.; Thomas Look, A.
    Autocrine activation of the MET receptor tyrosine kinase in acute myeloid leukemia (2012), Nat. Med., 18, 1118-1122.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine hepatocyte growth factor expression leads to autocrine activation of its receptor tyrosine kinase, MET, in nearly half of the acute myeloid leukemia cell lines and clinical samples studied. Genetic depletion of hepatocyte growth factor or MET potently inhibits the growth and survival of hepatocyte growth factor-expressing acute myeloid leukemia cells. Leukemic cells treated with the specific MET kinase inhibitor crizotinib develop resistance due to compensatory upregulation of hepatocyte growth factor expression, leading to restoration of MET signaling. In cases of acute myeloid leukemia where MET is coactivated with other tyrosine kinases, such as fibroblast growth factor receptor 1, concomitant inhibition of FGFR1 and MET blocks compensatory hepatocyte growth factor upregulation, resulting in sustained logarithmic cell kill both in vitro and in xenograft models in vivo Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P08581 MET
-

Synonyms

Synonyms Comment Organism
hepatocyte growth factor receptor
-
Homo sapiens
MET
-
Homo sapiens

General Information

General Information Comment Organism
physiological function hepatocyte growth factor expression leads to autocrine activation of its receptor tyrosine kinase, MET, in nearly half of the acute myeloid leukemia cell lines and clinical samples studied. Genetic depletion of hepatocyte growth factor or MET potently inhibits the growth and survival of hepatocyte growth factor-expressing acute myeloid leukemia cells. Leukemic cells treated with the specific MET kinase inhibitor crizotinib develop resistance due to compensatory upregulation of hepatocyte growth factor expression, leading to restoration of MET signaling. In cases of acute myeloid leukemia where MET is coactivated with other tyrosine kinases, such as fibroblast growth factor receptor 1, concomitant inhibition of FGFR1 and MET blocks compensatory hepatocyte growth factor upregulation, resulting in sustained logarithmic cell kill both in vitro and in xenograft models in vivo Homo sapiens