Activation of the cyclic AMP cascade as an oncogenic mechanism: the thyroid example

Biochimie. 1991 Jan;73(1):29-36. doi: 10.1016/0300-9084(91)90070-h.

Abstract

Three cascades activate thyroid cell proliferation: the EGF-protein tyrosine kinase pathway, the phorbol ester-protein kinase C pathway and the thyrotropin-cyclic AMP pathway. While the first 2 cascades converge early, they remain distinct from the cyclic AMP cascade until very late in G1. The cyclic AMP cascade is characterized by an early and transient expression of c-myc, which may explain why it induces proliferation and differentiation expression. Constitutive activation of this cascade causes growth and hyperfunction, ie, hyperfunctioning adenomas. The various possible defects that could lead to such a constitutive activation are discussed.

Publication types

  • Review

MeSH terms

  • Adenoma / etiology
  • Animals
  • Cell Division
  • Cyclic AMP / metabolism*
  • GTP-Binding Proteins / metabolism
  • Graves Disease / etiology
  • Humans
  • Protein Kinases / metabolism
  • Proto-Oncogenes*
  • Second Messenger Systems / physiology
  • Thyroid Gland / cytology
  • Thyroid Gland / metabolism*
  • Thyroid Neoplasms / etiology
  • Thyrotropin / physiology

Substances

  • Thyrotropin
  • Cyclic AMP
  • Protein Kinases
  • GTP-Binding Proteins