HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Roger, P. P Articles by Dumont, J. E Search for Related Content PubMed Articles by Roger, P. P Articles by Dumont, J. E

Thyrotropin-dependent insulin-like growth factor I mRNA expression in thyroid cells

Insulin-like growth factors regulate growth, differentiation and the maintenance of differentiated functions in numerous cell types. Insulin-like growth factor I (IGF-I) is produced in largest amounts as a circulating hormone by the liver in response to GH. However, the widespread distribution of IGF-I receptors and the production and secretion of IGF-I by almost all tissues suggest that IGF-I uses autocrine and paracrine modes of action, in addition to its endocrine effects (1). The almost ubiquitous activity of IGF-I in stimulating, if not triggering, cell proliferation is well illustrated by the almost general requirement of IGF-I (or high supra-physiological insulin concentrations that activate IGF-I receptors) as a supplement of serum-free culture media for most normal cell types (2). Cancer cells often escape the dependence for exogenous IGF-I because they secrete high levels of IGF-I in response to the transformation by various oncogenes (3). In the mouse embryo fibroblast model, the synergistic

This article has been cited by other articles:

				K. Krohn and R. Paschke Progress in Understanding the Etiology of Thyroid Autonomy J. Clin. Endocrinol. Metab., July 1, 2001; 86(7): 3336 - 3345. [Full Text] [PDF]