title: Increased ratio of mRNA expression of the genes CYP17 and CYP11B1 indicates autonomous cortisol production in adrenocortical tumors.
abstract: OBJECTIVE
  Due to increased use of imaging techniques, adrenal incidentalomas are frequently detected. The majority are non-hyperfunctioning adrenocortical tumors. We have previously shown that expression of the gene CYP17, coding for the enzyme in the cortisol pathway, correlates with cortisol release from adrenocortical tumors in vitro. The aim of this study was to compare clinical data with mRNA expression of CYP17 and CYP11B1 in adrenocortical tumors from patients with and without Cushing's syndrome and to identify adrenal tumors that may cause subclinical Cushing's syndrome.
  
  
  METHODS
  A retrospective study of 34 patients undergoing adrenalectomy due to an adrenal tumor.
  
  
  METHODS
  Clinical data were collected. In the adrenal gland the mRNA expression of the genes CYP17 and CYP11B1 was studied with in situ hybridisation technique.
  
  
  RESULTS
  The median ratio of CYP17/CYP11B1 expression in tumors from patients with Cushing's syndrome was significantly higher than the median ratio in the non-hyperfunctioning tumors. Tumors from 2 patients with subclinical Cushing's syndrome had ratios within the upper range for non-hyperfunctioning tumors.
  
  
  CONCLUSIONS
  The ratio between the expression of the genes CYP17 and CYP11B1 in tumors from patients with Cushing's syndrome is significantly higher than in the non-hyperfunctioning tumors. This indicates that 17alpha-hydroxylase is a major determinant of cortisol overproduction. The patients with subclinical Cushing's syndrome in this study are too few to draw any firm conclusions although the results suggest that subclinical Cushing's syndrome may be identified post-operatively with this method.
authors: Department of Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital Solna, SE - 171 76 Stockholm, Sweden.
authors: U
authors: U
authors: Enberg
authors: J
authors: J
authors: Hennings
authors: C
authors: C
authors: Volpe
authors: P
authors: P
authors: Hellman
authors: A
authors: A
authors: Höög
authors: B
authors: B
authors: Hamberger
authors: M
authors: M
authors: Thorén
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism*; D000315:Adrenalectomy; D018246:Adrenocortical Adenoma / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood / Q000652:urine; D003480:Cushing Syndrome / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis* / Q000097:blood / Q000652:urine; D017403:In Situ Hybridization; D033162:Incidental Findings; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics; D012189:Retrospective Studies; D018709:Statistics, Nonparametric; D013252:Steroid 11-beta-Hydroxylase / Q000235:genetics*; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics*
chemical_list: D012333:RNA, Messenger; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D013254:Steroid 17-alpha-Hydroxylase; D013252:Steroid 11-beta-Hydroxylase; D006854:Hydrocortisone