Key result
PDE11A expression is increased in primary pigmented nodular adrenocortical disease, and PDE11A defects are associated with high CREB phosphorylation similar to PRKAR1A mutations.
Observational (n=22)
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PDE11A defects may contribute to PPNAD pathogenesis; leaves open whether PDE11A represents a therapeutic target in adrenal Cushing syndrome.
Boikos et al. (2008) conducted an observational in Adrenal tumors and bilateral adrenocortical hyperplasias (n=22). Adrenocortical tumors and specific genetic mutations (PDE11A, PRKAR1A, GNAS) vs. Normal adrenocortical tissue was evaluated on PDE11A expression and phosphorylated CREB levels. PDE11A expression is increased in primary pigmented nodular adrenocortical disease, and PDE11A defects are associated with high CREB phosphorylation similar to PRKAR1A mutations.
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