MM-131, a bispecific anti-Met/EpCAM mAb, inhibits HGF-dependent and HGF-independent Met signaling through concurrent binding to EpCAM

Activation of the Met receptor tyrosine kinase, either by its ligand, hepatocyte growth factor (HGF), or via ligand-independent mechanisms, such as MET amplification or receptor overexpression, has been implicated in driving tumor proliferation, metastasis, and resistance to therapy. Clinical develo...

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Dades bibliogràfiques
Publicat a:Proc Natl Acad Sci U S A
Autors principals: Casaletto, Jessica B., Geddie, Melissa L., Abu-Yousif, Adnan O., Masson, Kristina, Fulgham, Aaron, Boudot, Antoine, Maiwald, Tim, Kearns, Jeffrey D., Kohli, Neeraj, Su, Stephen, Razlog, Maja, Raue, Andreas, Kalra, Ashish, Håkansson, Maria, Logan, Derek T., Welin, Martin, Chattopadhyay, Shrikanta, Harms, Brian D., Nielsen, Ulrik B., Schoeberl, Birgit, Lugovskoy, Alexey A., MacBeath, Gavin
Format: Artigo
Idioma:Inglês
Publicat: National Academy of Sciences 2019
Matèries:
PNAS Plus
Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC6462049/
https://ncbi.nlm.nih.gov/pubmed/30898885
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.1819085116
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