title: Absence of somatostatin receptor type 2 A mutations and gip oncogene in pituitary somatotroph adenomas.
abstract: OBJECTIVE
  Somatostatin, acting via specific receptors in the anterior pituitary, tonically inhibits pituitary growth hormone secretion and somatotroph proliferation. Reduction of growth hormone secretion and tumour regression in GH-secreting pituitary adenomas treated with long-acting somatostatin analogues varies widely. In 30-40% of these tumours dominant somatic mutations of the Gsalpha gene (gsp) have been demonstrated leading to constitutive adenylyl cyclase induction. A relationship between somatostatin sensitivity and tumour pathogenesis in some tumours has been suggested. Changes in the function of the somatostatin receptor or intracellular signal elements may be of relevance. Somatostatin receptor type 2 A (sst2A) and Gi2 are proposed to mediate selectively the inhibition of GH release in the somatotroph. We therefore investigated the presence of sst2A mutations and gip oncogene in somatotrophic pituitary adenomas.
  
  
  METHODS
  Tumour samples from 15 patients with pituitary somatotroph adenomas were obtained. RNA was isolated and used for reverse transcription and subsequent polymerase chain reaction. All samples were screened for the presence of sst2A mutations and of the gip oncogene by SSCP analysis and sequencing. For comparison, the gsp oncogene was examined. The relationship between clinical data and molecular analysis results was investigated.
  
  
  RESULTS
  Seven of the tumours harboured a gsp mutation. No mutations affecting the sst2A protein were found in any of the tumours analysed. Furthermore, gip oncogene was absent in all tumours.
  
  
  CONCLUSIONS
  Mutations of the somatostatin receptor type 2 A and the gip oncogene are unlikely to be involved in the pathogenesis of acromegaly.
authors.affiliation: IHF Institute for Hormone and Fertility Research, University of Hamburg, Hamburg, Germany; Department of Medicine, University Hospital Eppendorf, Hamburg, Germany. petersenn@uke.uni-hamburg.de
authors.forename: S
authors.initials: S
authors.lastname: Petersenn
authors.forename: M
authors.initials: M
authors.lastname: Heyens
authors.forename: D K
authors.initials: DK
authors.lastname: Lüdecke
authors.forename: F U
authors.initials: FU
authors.lastname: Beil
authors.forename: H M
authors.initials: HM
authors.lastname: Schulte
mesh_terms: D000236:Adenoma / Q000235:genetics / Q000378:metabolism*; D004252:DNA Mutational Analysis; D019382:Human Growth Hormone / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D009857:Oncogenes; D010911:Pituitary Neoplasms / Q000235:genetics / Q000556:secondary*; D018807:Polymorphism, Single-Stranded Conformational; D017481:Receptors, Somatostatin / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D017481:Receptors, Somatostatin; D019382:Human Growth Hormone; C093733:somatostatin receptor 2