adrenocortical adenoma/グルタチオン

Immunocytochemical localization of glutathione-peroxidase (GSH-PO) in human adrenal glands was studied on adrenocortical adenomas associated with primary aldosteronism and Cushing's syndrome. Normal adrenal glands were obtained from non-adenomatous regions of the same surgical specimens. In the

Benign adrenocortical adenoma is a major primary cause of Cushing's syndrome. Although numerous studies have been performed, the molecular mechanism of adrenocortical adenoma is yet to be elucidated. In this study we endeavored to identify genes differentially regulated in adrenocortical adenoma by

BACKGROUND The cortisol secretion of adrenocortical adenomas can be either subtle or overt. The mechanisms leading to the autonomous hypersecretion of cortisol are unknown. OBJECTIVE The objective of the study was to identify the gene expression profile associated with the autonomous and excessive

BACKGROUND Adrenocortical tumors occur as sporadic tumors, as part of the multiple endocrine neoplasia type 1 (MEN1) syndrome, or as part of other hereditary disorders. MEN1 is a tumor suppressor gene located on chromosome 11q13 that encodes a 610-amino acid protein called menin, and plays an

Chicken ovalbumin upstream promoter-transcription factors (COUP-TFs) are orphan receptors involved in regulation of neurogenesis and organogenesis. COUP-TF family members are generally considered to be transcriptional repressors and several mechanisms have been proposed to underlie this activity. To