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Titolo:
G(S) PROTEIN MUTATIONS AND PITUITARY-TUMORS - FUNCTIONAL CORRELATES AND POSSIBLE THERAPEUTIC IMPLICATIONS
Autore:
FAGLIA G; AROSIO M; SPADA A;
Indirizzi:
UNIV MILAN,INST ENDOCRINE SCI,OSPED MAGGIORE,IRCCS,VIA F SFORZA 35 I-20122 MILAN ITALY UNIV MILAN,INST ENDOCRINE SCI I-20122 MILAN ITALY
Titolo Testata:
Metabolism, clinical and experimental
fascicolo: 8, volume: 45, anno: 1996, supplemento:, 1
pagine: 117 - 119
SICI:
0026-0495(1996)45:8<117:GPMAP->2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN ENDOCRINE TUMORS; GS-ALPHA; ACROMEGALIC PATIENTS; BIOCHEMICAL CHARACTERISTICS; ADENYLYL CYCLASE; CELL-CULTURE; GENE; ADENOMAS; CHAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
18
Recensione:
Indirizzi per estratti:
Citazione:
G. Faglia et al., "G(S) PROTEIN MUTATIONS AND PITUITARY-TUMORS - FUNCTIONAL CORRELATES AND POSSIBLE THERAPEUTIC IMPLICATIONS", Metabolism, clinical and experimental, 45(8), 1996, pp. 117-119

Abstract

In more than one third of growth hormone (GH)-secreting pituitary adenomas, a point mutation in the gene for the alpha-chain of the G stimulatory protein (gsp oncogene) causes the constitutive activation of the membrane adenylyl cyclase (AC) resulting in uncontrolled cyclic adenosine monophosphate (cAMP) elevation and GH hypersecretion. Tumors expressing gsp are characterized by high membrane AC activity, elevated intracellular cAMP content, and high rates of GH release in culture medium. The AC activity is not further stimulated by GH-releasing hormone(GHRH) and other specific and non-specific agents, while it is lowered by somatostatin, as the G inhibitory protein (G(i)) is normally working. Acromegalic patients bearing adenomas with the gsp mutation do not present with any obvious clinical or epidemiological distinctive features. However, they have smaller tumors in relation to their circulating GH levels, suggesting that the gsp oncogene maintains a high late of secretory activity in vivo. Most of these patients show paradoxicalGH increases to thyrotropin-releasing hormone (TRH). but none to gonadotropin-releasing hormone (GnRH) or an oral glucose tolerance test (OGTT). As with the in vitro data, these patients are not very sensitiveto GHRH administration, but are sensitive to the inhibitory action ofsomatostatin. In our experience, only three of six patients with non-gsp-mutated tumors had lowered serum GH levels during the administration of octreotide (100 mu g thrice daily for 4 years), while all of sixpatients with gsp-mutated tumors had serum GH levels suppressed by octreotide treatment. Such a good GH suppressibility by somatostatin makes patients with gsp-mutated tumors the best candidates for medical treatment with somatostatin analogs. Copyright (C) 1996 by W.B. SaundersCompany

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Documento generato il 24/11/20 alle ore 10:49:14