Abstract
BackgroundCalcitonin 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.MethodsCalcitonin 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.ResultsCalcitonin 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 RET/RAS genes and absence of tumor stroma, suggesting that CTR expression do not associate with clinicopathological signs of worse prognosis.DiscussionCalcitonin receptor expression appears to be associated in MTC with more differentiated status of the neoplastic cells.
Highlights
Medullary thyroid carcinoma (MTC) is a rare tumor representing 5–10% of thyroid cancers (Elisei et al, 2013)
calcitonin receptor (CTR) protein expression in medullary thyroid carcinoma (MTC) Calcitonin receptor expression was mainly localized in the cytoplasm and was detected in 62 out of 75 samples (82.7%), while the remaining 13 samples (17.3%) were negative
In the 62 positive samples, CTR expression was present in more than 50% of the cells in 55 cases (88.7%) (Table 1) and the staining intensity was faint in 34.7%, moderate in 25.3% and strong in 25.3% (Table 1)
Summary
Medullary thyroid carcinoma (MTC) is a rare tumor representing 5–10% of thyroid cancers (Elisei et al, 2013) It is a tumor with neuroendocrine differentiation and arises from the parafollicular C-cells of the thyroid which normally secrete calcitonin (CT). MTC originates as a sporadic (75–80%) malignancy or a manifestation of hereditary syndromes (20–25%), i.e., multiple endocrine neoplasia type 2 (MEN2A or MEN2B)/ familial MTC, with an autosomal dominant pattern due to germline mutations of the RET gene (Pacini et al, 2010) In both forms of MTC (sporadic and familial) the cliniclaboratorial diagnosis is based mainly on the finding of elevated levels of serum CT, in basal and stimulated conditions. Discussion: Calcitonin receptor expression appears to be associated in MTC with more differentiated status of the neoplastic cells
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