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Calcitonin receptor expression in medullary thyroid carcinoma

Calcitonin expression is a well-established marker for medullary thyroid carcinoma (MTC); yet the role of calcitonin receptor (CTR), its seven-transmembrane G-protein coupled receptor, remains to be established in C-cells derived thyroid tumors. The aim of this work was to investigate CTR expression...

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Published in:PeerJ (San Francisco, CA) CA), 2017-09, Vol.5, p.e3778-e3778, Article e3778
Main Authors: Cappagli, Virginia, Potes, Catarina Soares, Ferreira, Luciana Bueno, Tavares, Catarina, Eloy, Catarina, Elisei, Rossella, Sobrinho-Simões, Manuel, Wookey, Peter J, Soares, Paula
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Language:English
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Summary:Calcitonin expression is a well-established marker for medullary thyroid carcinoma (MTC); yet the role of calcitonin receptor (CTR), its seven-transmembrane G-protein coupled receptor, remains to be established in C-cells derived thyroid tumors. The aim of this work was to investigate CTR expression in MTC and to correlate such expression with clinicopathological features in order to evaluate its possible role as a prognostic indicator of disease aggressiveness and outcome. Calcitonin receptor expression was analyzed in a series of 75 MTCs by immunohistochemistry, and by qPCR mRNA quantification in specimens from four patients. Statistical tests were used to evaluate the correlation between CTR expression and the clinicopathological and molecular characteristics of patients and tumors. Calcitonin receptor expression was detected in 62 out of 75 samples (82.7%), whereas 13 of the 75 samples (17.3%) were completely negative. CTR expression was significantly associated with expression of cytoplasmatic phosphatase and tensin homologue deleted on chromosome 10 and osteopontin, as well as with wild type genes and absence of tumor stroma, suggesting that CTR expression do not associate with clinicopathological signs of worse prognosis. Calcitonin receptor expression appears to be associated in MTC with more differentiated status of the neoplastic cells.
ISSN:2167-8359
2167-8359
DOI:10.7717/peerj.3778