IndraLab
Statements
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"Cross-talk between EGFR and c-Met in lung cancer, including EGFR-dependent phosphorylation and activation of c-Met through EGFR ligands, has been widely reported. xref Because of this cross-talk and link between EGFR TKI resistance and c-Met activation, simultaneous targeting of these 2 pathways holds promise. xref Multiple studies have highlighted the use of EGFR and c-Met combination treatments, as well as single, dual targeting therapeutics. xref In response to this need, we designed JNJ-61186372 as a bispecific antibody to dually target EGFR and c-Met. xref "
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"Several groups have investigated the molecular mechanisms underlying the crosstalk between EGFR and c-Met, and it has become apparent that several partner proteins can affect EGFR mediated phosphorylation of c-Met, including Src, MAPK and beta1 integrins [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"It has been demonstrated that EGFR activation contributes to c-Met tyrosine phosphorylation in a variety of cell models, with varying kinetic parameters Since NSCLC commonly express both receptors, we examined whether EGFR ligands induce c-Met phosphorylation in human NSCLC cell lines."
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"VK3 induced phosphorylation of hepatocyte growth factor receptor (c-met), epidermal growth factor receptor (EGFR), or external signal regulated kinase (ERK), which increased progressively to a maximum level at 30 minutes, in a dose dependent manner and occurred at growth inhibitory concentrations."