Etiology of acromegaly

A molecular biological approach

A. Spada, M. Bassetti, P. Gil-del-Alamo, K. Saccomanno, A. Lania

Research output: Contribution to journalArticle

Abstract

Acromegalic patients with gsp oncogene show a progression of the disease similar to that characterizing patients without this alteration. The low rate of tumor growth has been confirmed by long-term (up to 10 years) follow-up evaluation; in this study, no recurrence of adenoma with the gsp oncogene is reported. These data correlate well with the poor morphological evidence for cell replication in tumors expressing gsp mutations. In fact, from morphological studies these adenomas appear to be made up of densely granulated cells with a well-developed secretory apparatus, without detectable mitoses. Therefore, according to morphological parameters, tumors expressing the gsp oncogene seem to belong to the so-called densely granulated adenomas, which are generally considered less invasive growth hormone (GH)-secreting adenomas. Moreover, these patients are reported to be extremely sensitive to the inhibitory action of somatostatin, which reduces GH release in normal and tumoral somatotropes by inhibiting cyclic adenosine monophosphate (cAMP) production. This suggests that the expression of oncogenic mutations might be partially counteracted in vivo by inhibitory agents. Further studies are required to determine which activating mutations other than gsp may occur, whether these mutations occur as an early or late step, and what the role of tumor suppressor gene is in GH-secreting adenoma formation. Finally, the reason that almost all GH-secreting tumors histologically remain benign still eludes investigators.

Original languageEnglish
Pages (from-to)31-33
Number of pages3
JournalMetabolism
Volume44
Issue numberSUPPL. 1
DOIs
Publication statusPublished - 1995

Fingerprint

Acromegaly
Adenoma
Growth Hormone
Oncogenes
Mutation
Neoplasms
Somatostatin
Tumor Suppressor Genes
Mitosis
Cyclic AMP
Disease Progression
Research Personnel
Recurrence
Growth

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Spada, A., Bassetti, M., Gil-del-Alamo, P., Saccomanno, K., & Lania, A. (1995). Etiology of acromegaly: A molecular biological approach. Metabolism, 44(SUPPL. 1), 31-33. https://doi.org/10.1016/0026-0495(95)90308-9

Etiology of acromegaly : A molecular biological approach. / Spada, A.; Bassetti, M.; Gil-del-Alamo, P.; Saccomanno, K.; Lania, A.

In: Metabolism, Vol. 44, No. SUPPL. 1, 1995, p. 31-33.

Research output: Contribution to journalArticle

Spada, A, Bassetti, M, Gil-del-Alamo, P, Saccomanno, K & Lania, A 1995, 'Etiology of acromegaly: A molecular biological approach', Metabolism, vol. 44, no. SUPPL. 1, pp. 31-33. https://doi.org/10.1016/0026-0495(95)90308-9
Spada A, Bassetti M, Gil-del-Alamo P, Saccomanno K, Lania A. Etiology of acromegaly: A molecular biological approach. Metabolism. 1995;44(SUPPL. 1):31-33. https://doi.org/10.1016/0026-0495(95)90308-9
Spada, A. ; Bassetti, M. ; Gil-del-Alamo, P. ; Saccomanno, K. ; Lania, A. / Etiology of acromegaly : A molecular biological approach. In: Metabolism. 1995 ; Vol. 44, No. SUPPL. 1. pp. 31-33.
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