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REarranged during Transfection proto-oncogene (RET)
- Target
- RET
- Molecular classification
- Receptor Tyrosine Kinase, Receptor
01
Overview
The RET proto-oncogene encodes a receptor tyrosine kinase crucial for neural crest development, kidney morphogenesis, and nervous system formation. Activation requires dimerization via GDNF family ligands and GFRα coreceptors, leading to autophosphorylation and downstream signaling. Gain-of-function mutations or rearrangements cause constitutive activation, driving cancers like thyroid carcinoma and multiple endocrine neoplasia. Conversely, loss-of-function mutations lead to Hirschsprung’s disease. RET is a therapeutic target, with ongoing development and clinical use of selective small-molecule inhibitors.
- Other names
- RET51RET43RET9
02
Mechanism of action
RET inhibitors target the ATP-binding site of the RET kinase domain, preventing autophosphorylation and downstream signaling.
03
Biological functions
Signal transductionCell proliferationCell migrationCell differentiationCell survivalNeuronal navigationKidney morphogenesisEnteric nervous system formationNeural crest development
04
Disease associations
Papillary thyroid carcinomaMultiple endocrine neoplasia type 2A (MEN2A)Multiple endocrine neoplasia type 2B (MEN2B)Medullary thyroid carcinomaPheochromocytomaParathyroid hyperplasiaHirschsprung’s diseaseCancer
05
Safety considerations
Off-target effects of RET inhibitorsDevelopment of resistance to RET inhibitorsToxicities associated with kinase inhibition
06
Interacting drugs
RET inhibitors (small-molecule inhibitors)
07
Biomarkers
RET mutations/fusions in tumor tissue (for patient selection)RET phosphorylation levels (for efficacy monitoring)
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