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Expression of cAMP-responsive element binding protein and inducible cAMP early repressor in hyperfunctioning thyroid
Alessandro Peri1, Paola Luciani, Massimo Tonacchera
1Endocrine Unit, Department of Clinical Physiopathology, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy. a.peri@dfc.unifi.it
European Journal of Endocrinology
|June 1, 2002
Summary
Thyroid hyperfunctioning adenomas show no significant difference in CREB and ICER gene expression between tumor and normal tissue. These findings suggest complex molecular mechanisms in adenoma pathogenesis beyond simple cAMP pathway activation.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid hyperfunctioning adenomas pathogenesis is not fully understood.
- Gain-of-function mutations in TSH receptor or G(s)alpha gene, activating the cAMP pathway, are debated.
- CREB and ICER are nuclear transcription factors downstream of cAMP signaling.
Purpose of the Study:
- To investigate the expression of CREB and ICER genes in thyroid hyperfunctioning adenomas.
- To compare gene expression in nodular versus extranodular thyroid tissue.
- To correlate gene expression with TSH receptor and G(s)alpha gene mutation status.
Main Methods:
- RT-PCR and Western blot analysis were performed on 14 patients.
- Direct sequencing was used to identify mutations in TSH receptor and G(s)alpha genes.
- Quantitative analysis of CREB and ICER transcripts and protein levels was conducted.
Main Results:
- No significant difference in CREB transcript or protein levels was found between adenomas and normal thyroid tissue.
- No significant difference in ICER transcript levels was observed between adenomas and normal thyroid tissue.
- These findings were consistent regardless of TSH receptor gene mutation status.
Conclusions:
- The study does not support a simple model of cAMP pathway activation in all hyperfunctioning adenomas.
- Results suggest that counteracting molecular mechanisms may be involved in adenoma pathogenesis.
- Complex pathways likely contribute to the development of hyperfunctioning thyroid tumors.