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Related Experiment Videos

Cellular abnormalities in pituitary tumors

A Spada1, A Lania, S Mantovani

  • 1Institute of Endocrine Sciences, Ospedale Maggiore IRCCS, University of Milan, Italy.

Metabolism: Clinical and Experimental
|August 1, 1996
PubMed
Summary
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Pituitary tumors may grow due to cyclic adenosine monophosphate (cAMP) signaling. Altered hormone receptors can disrupt normal inhibitory signals, potentially amplifying tumor growth and hormone secretion.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Pituitary cell proliferation is linked to cyclic adenosine monophosphate (cAMP) signaling, a key factor in tumorigenesis.
  • Normal pituitary function relies on a balance between stimulatory neurohormones and inhibitory inputs that regulate cAMP levels.
  • Alterations in hormone receptors and postreceptor pathways can disrupt this balance, contributing to pituitary adenomas.

Purpose of the Study:

  • To investigate the role of receptor/postreceptor alterations in pituitary tumorigenesis.
  • To explore the signaling pathways of various peptides and inhibitory agents in different pituitary adenoma subtypes.
  • To understand how abnormal receptor expression contributes to amplified stimulatory signals and tumor growth.

Main Methods:

Related Experiment Videos

  • Analysis of thyrotropin-releasing hormone (TRH) receptors in various pituitary adenomas.
  • Assessment of sensitivity to vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating peptide (PACAP).
  • Evaluation of the effects of somatostatin (SS) and dopamine (DA) on hormone secretion and tumor growth, including intracellular calcium ([Ca2+]i) and adenylyl cyclase activity.

    • Main Results:

    • Most pituitary adenomas (GH, ACTH, PRL, gonadotropin-secreting, and NFPA) express TRH receptors coupled with increased cytosolic calcium and diacylglycerol production.
    • Many adenomas and all NFPAs are sensitive to VIP and PACAP, which activate adenylyl cyclase.
    • Dopamine (DA) signaling is defective in GH-secreting adenomas, leading to impaired adenylyl cyclase inhibition and only reduced cytosolic calcium.
    • In a subset of NFPAs, SS or DA can paradoxically increase cytosolic calcium due to intracellular calcium mobilization.
    • Abnormal receptor expression can amplify stimulatory signals, promoting both hormone secretion and cell proliferation.

    Conclusions:

    • Aberrant signaling pathways, particularly involving cAMP and intracellular calcium, are implicated in pituitary adenoma development and progression.
    • Dysfunctional dopamine and somatostatin signaling contribute to uncontrolled pituitary cell growth and hormone hypersecretion.
    • Understanding these molecular mechanisms offers potential targets for therapeutic interventions in pituitary tumors.