Activation of the cyclic AMP cascade as an oncogenic mechanism: the thyroid example.
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.
Maenhaut
C
C
Institut de Recherche Interdisciplinaire, Faculté de Médecine, Hôpital Erasme, Université Libre de Bruxelles, Belgium.
Roger
P P
PP
Reuse
S
S
Dumont
J E
JE
D000236:Adenoma / Q000209:etiology; D000818:Animals; D002455:Cell Division; D000242:Cyclic AMP / Q000378:metabolism*; D019204:GTP-Binding Proteins / Q000378:metabolism; D006111:Graves Disease / Q000209:etiology; D006801:Humans; D011494:Protein Kinases / Q000378:metabolism; D011519:Proto-Oncogenes; D015290:Second Messenger Systems / Q000502:physiology; D013961:Thyroid Gland / Q000166:cytology / Q000378:metabolism*; D013964:Thyroid Neoplasms / Q000209:etiology; D013972:Thyrotropin / Q000502:physiology
D013972:Thyrotropin; D000242:Cyclic AMP; D011494:Protein Kinases; D019204:GTP-Binding Proteins