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The human *RET* proto-oncogene encodes a unique receptor tyrosine kinase crucial for neural development but also implicated in several aggressive cancers when mutated or rearranged. Its complex activation mechanism involves both ligand binding from the GDNF family and interaction with specific coreceptors—a feature distinguishing it from many other RTKs. Both loss-of-function mutations leading to developmental disorders like Hirschsprung disease and gain-of-function mutations driving oncogenesis highlight its clinical significance as a therapeutic target.
Inhibition of RET tyrosine kinase activity, blocking downstream signaling pathways (RAS-MAPK/ERK1/2, PI3K-AKT)
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