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Based on this, our results suggest that the sequence of modulatory effects on glucose metabolic homeostasis exhibited by the binding of GLP-1 to its receptor are possibly influenced, to a greater extent, by the interaction of GLP-1 with its pancreatic receptor and are less dependent on interaction with hepatic GLP-1R

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showed that dual blockade of SU11274 (c-MET inhibitor) and erlotinib (EGFR inhibitor) in HNSCC lines produce greater-than-additive inhibition of cell growth via erbB3/AKT signaling [86]