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Cushing's syndrome is a critical state of endogenous hypercortisolemia with metabolic, cardiovascular, and musculoskeletal complications that requires surgical or medical treatment
Cushing's syndrome is a critical state of endogenous hypercortisolemia with metabolic, cardiovascular, and musculoskeletal complications that requires surgical or medical treatment
The cause is a germline inactivating mutation of PRKAR1A (a regulatory unit of PKA) or phosphodiesterase 11A (PDE11A)
Methods: Fifty-seven patients with CPA underwent adrenalectomy at Seoul National University Hospital
Results: The incidence of PRKACA L206R mutation was 51% (29/57)
Table 1 Clinical and biochemical characteristics of subjects according to PRKACA somatic mutation status
Table 1 Clinical and biochemical characteristics of subjects according to PRKACA somatic mutation statusAnalysis of differentially expressed genes (DEGs) between protein kinase camp-activated catalytic subunit alpha (PRKACA) L206R mutant and wild-type cortisol-producing adenomas (CPAs) (A) V volcano plot of DEGs with PRKACA L206R mutation on the x-axis The magnitude of the difference in gene expression between body and wild-type CPAs, and the y-axis is the statistical significance of the difference
Analysis of differentially expressed genes (DEGs) between protein kinase camp-activated catalytic subunit alpha (PRKACA) L206R mutant and wild-type cortisol-producing adenomas (CPAs) (A) V volcano plot of DEGs with PRKACA L206R mutation on the x-axis The magnitude of the difference in gene expression between body and wild-type CPAs, and the y-axis is the statistical significance of the difference
Table 2 The main differentially expressed genes of PRKACA L206R mutant and wild-type cortisol adenomas (|FC|≥2, P<0.
Table 2 The main differentially expressed genes of PRKACA L206R mutant and wild-type cortisol adenomas (|FC|≥2, P<0.
Transcriptome analysis supported that the PRKACA L206R mutation in CPAS resulted in increased hormone activity and limited proliferative capacity
Clinical and Molecular Characteristics of PRKACA L206R Mutant Cortisol-Producing Adenomas in Korean Patients.
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