Cellular abnormalities in pituitary tumors

Anna Spada, Andrea Lania, Simona Mantovani

Research output: Contribution to journalArticle

Abstract

Pituitary cells appear to be programmed to proliferate in response to cyclic adenosine monophosphate (cAMP), leading to tumorigenesis. Stimulatory neurohormones and inhibitory inputs normally act in opposition to control cAMP levels, but receptor/postreceptor alterations may affect their relative effects. Most growth hormone (GH), corticotropin (ACTH)-, prolactin (PRL)-, and gonadotropin-secreting adenomas and nonfunctioning pituitary adenomas (NFPA) possess specific thyrotropin-releasing hormone (TRH) receptors, normally coupled with cytosolic [Ca2+]i increase and diacyl glycerol production. These cells are also sensitive to other peptides such as vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating peptide (PACAP), which activate adenylyl cyclase in many hormone-secreting adenomas and in all NFPA. The two main inhibitory agents controlling pituitary function are somatostatin (SS) and dopamine (DA), which have been reported to reduce hormone hypersecretion and tumor growth in a variable percentage of patients. Inhibition of adenylyl cyclase activity and cytosolic [Ca2+]i levels is involved in the transduction of DA signals in normal and tumoral mammotrophs, but in GH-secreting adenomas DA receptors are exclusively and defectively coupled only with [Ca2+]i reduction. The abnormal expression of these receptors can amplify stimulatory signals with both secretory and proliferative potential. The availability of specific G proteins may qualify the cell response to inhibitory agents. For example, in a subset of NFPA, SS alone or DA alone causes an abnormal increase in [Ca2+]i levels due to Ca2+ mobilization from intracellular stores.

Original languageEnglish
Pages (from-to)46-48
Number of pages3
JournalMetabolism
Volume45
Issue numberSUPPL.1
Publication statusPublished - 1996

Fingerprint

Pituitary Neoplasms
Adenylyl Cyclases
Adenoma
Dopamine
Somatostatin
Cyclic AMP
Adrenocorticotropic Hormone
Growth Hormone
Thyrotropin Releasing Hormone Receptors
Hormones
Peptides
Vasoactive Intestinal Peptide
Dopamine Receptors
Gonadotropins
GTP-Binding Proteins
Prolactin
Glycerol
Neurotransmitter Agents
Signal Transduction
Carcinogenesis

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Spada, A., Lania, A., & Mantovani, S. (1996). Cellular abnormalities in pituitary tumors. Metabolism, 45(SUPPL.1), 46-48.

Cellular abnormalities in pituitary tumors. / Spada, Anna; Lania, Andrea; Mantovani, Simona.

In: Metabolism, Vol. 45, No. SUPPL.1, 1996, p. 46-48.

Research output: Contribution to journalArticle

Spada, A, Lania, A & Mantovani, S 1996, 'Cellular abnormalities in pituitary tumors', Metabolism, vol. 45, no. SUPPL.1, pp. 46-48.
Spada A, Lania A, Mantovani S. Cellular abnormalities in pituitary tumors. Metabolism. 1996;45(SUPPL.1):46-48.
Spada, Anna ; Lania, Andrea ; Mantovani, Simona. / Cellular abnormalities in pituitary tumors. In: Metabolism. 1996 ; Vol. 45, No. SUPPL.1. pp. 46-48.
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