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Absence of somatostatin receptor type 2 A mutations and gip oncogene in pituitary somatotroph adenomas

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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 Gsα 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. DESIGN

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. CONCLUSION

Mutations of the somatostatin receptor type 2 A and the gip oncogene are unlikely to be involved in the pathogenesis of acromegaly.
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Document Type: Research Article

Affiliations: 1: IHF Institute for Hormone and Fertility Research, University of Hamburg, Hamburg, Germany 2: Department of Neurosurgery, University Hospital Eppendorf, 20246 Hamburg, Germany

Publication date: January 1, 2000

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