Document Detail

Expression of cAMP-responsive element binding protein and inducible cAMP early repressor in hyperfunctioning thyroid adenomas.
MedLine Citation:
PMID:  12039695     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The pathogenesis of thyroid hyperfunctioning adenomas is still only partially understood and controversy exists about the frequency of gain-of-function mutations of the TSH receptor or G(s)alpha gene, which activate the cAMP pathway. The nuclear transcription factors cAMP-responsive element binding protein (CREB) and inducible cAMP early repressor (ICER) are among the final targets of this signalling cascade. DESIGN: In our study we focused on the expression of CREB and ICER genes in the nodular as well as in the extranodular tissue of hyperfunctioning tumours of the thyroid. METHODS: RT-PCR and Western blot analysis were performed in a series of 14 patients. The presence of an activating mutation of the TSH receptor or of the G(s)alpha gene was ascertained by direct sequencing. RESULTS: The levels of CREB transcripts did not significantly differ in the adenomas and in the normal tissues (CREB/GAPDH, mean optical density+/-s.e.: 0.98+/-0.18 vs 0.88+/-0.27 respectively, P = not significant (N.S.)), although case-to-case variability was observed. The absence of a significant difference between the adenoma and the surrounding normal tissue was maintained after dividing the patients into two groups, according to TSH receptor status. Accordingly, no significant difference in the levels of CREB protein (total and Ser(133)-phosphorylated) was observed between the nodular and the extranodular tissue. In addition, no difference was found in the levels of ICER transcripts (ICER/GAPDH, mean optical density+/-s.e.: 0.52+/-0.11, nodule vs 0.36+/-0.11, normal thyroid, P=N.S.), independently of the TSH receptor gene status (i.e. wild-type or mutated). CONCLUSIONS: Our results support the recent hypothesis that the activation of the cAMP pathway in hyperfunctioning adenomas of the thyroid might be counteracted by opposite events and suggest that complex molecular mechanisms might take part in the pathogenesis of hyperfunctioning tumours.
Alessandro Peri; Paola Luciani; Massimo Tonacchera; Patrizia Agretti; Silvana Baglioni-Peri; Lisa Buci; Barbara Conforti; Federica Cioppi; Giancarlo Biliotti; Mario Serio; Paolo Vitti; Luca Chiovato
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of endocrinology / European Federation of Endocrine Societies     Volume:  146     ISSN:  0804-4643     ISO Abbreviation:  Eur. J. Endocrinol.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-05-31     Completed Date:  2002-07-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9423848     Medline TA:  Eur J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  759-66     Citation Subset:  IM    
Endocrine Unit, Department of Clinical Physiopathology, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy.
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MeSH Terms
Activating Transcription Factor 1
Adenoma / blood,  metabolism*
Blotting, Western
Chemiluminescent Measurements
Cyclic AMP / metabolism*
Cyclic AMP Response Element Modulator
DNA-Binding Proteins / biosynthesis*,  genetics
Gene Expression Regulation, Neoplastic
Middle Aged
RNA, Messenger / analysis
Receptors, Thyrotropin / genetics*
Repressor Proteins / biosynthesis*,  genetics
Reverse Transcriptase Polymerase Chain Reaction
Sequence Analysis, DNA
Signal Transduction
Thyroid Hormones / blood*
Thyroid Neoplasms / blood,  metabolism*
Transcription Factors / biosynthesis*,  genetics
Reg. No./Substance:
0/Activating Transcription Factor 1; 0/DNA-Binding Proteins; 0/RNA, Messenger; 0/Receptors, Thyrotropin; 0/Repressor Proteins; 0/Thyroid Hormones; 0/Transcription Factors; 135844-64-3/Cyclic AMP Response Element Modulator; 60-92-4/Cyclic AMP

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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