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Abstract Glucagon-like petide-1 (GLP-1) potentiates insulin and suppresses glucagon secretion from the pancreas in response to the ingestion of nutrients
In addition to the tumorigenic effects of succinate accumulation, SDH5 mutation is the key driver supporting the acquisition of epithelialmesenchymal transition (EMT) characteristics
The next major step in this therapeutic evolution is the addition of glucagon receptor activation
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