Sex-steroid hormone receptors in human medullary thyroid carcinoma.
ABSTRACT Three complementary techniques were used to detect sex-steroid hormone receptors in tumor tissues from seven patients with medullary thyroid carcinoma: steroid binding analysis, enzyme immune assay, and immunohistochemistry. The presence of estrogen receptors was detected by steroid binding analysis in one of seven patients, although in very low concentrations (3.17 to 5.06 fmol/mg protein). These results were confirmed by enzyme immune assay (6.35 to 9.32 fmol/mg protein). Progesterone receptors were found in five of seven patients by steroid binding analysis (11.1 to 47.9 fmol/mg protein), and progesterone receptor results were confirmed by enzyme immune assay (8.1 to 34.1 fmol/mg protein). By immunohistochemistry, progesterone receptors were focally detected in all cases, whereas all tumors were negative for estrogen receptors. In summary, our results confirm the presence of sex-steroid hormone receptors, particularly progesterone receptors in medullary thyroid carcinoma. The presence of progesterone receptors in medullary thyroid carcinoma apparently does not require the continuous presence of estrogen receptors.
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ABSTRACT: Thyroid diseases are more prevalent in women, particularly between puberty and menopause. It is wellknown that estrogen (E) has indirect effects on the thyroid economy. Direct effects of this steroid hormone on thyroid cells have been described more recently; so, the aim of the present paper was to review the evidences of these effects on thyroid function and growth regulation, and its mechanisms. The expression and ratios of the two E receptors, α and β, that mediate the genomic effects of E on normal and abnormal thyroid tissue were also reviewed, as well as nongenomic, distinct molecular pathways. Several evidences support the hypothesis that E has a direct role in thyroid follicular cells; understanding its influence on the growth and function of the thyroid in normal and abnormal conditions can potentially provide new targets for the treatment of thyroid diseases.05/2011; 2011:875125. DOI:10.4061/2011/875125
Journal of Korean Endocrine Society 01/2009; 24(2). DOI:10.3803/jkes.2009.24.2.93
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ABSTRACT: Medullary thyroid carcinoma (MTC) is an uncommon tumour of calcitonin-secreting C-cells of the thyroid gland. This cancer represents an important potential model for the study of mechanisms of human epithelial cell transformation. Although recent studies have identified the gene involved in familial forms of MTC, little is known about the molecular pathogenesis of the sporadic variants of this tumour. The biological and prognostic significance of TFF1 expression, particularly in diverse human malignancies, suggests that the TFF1 protein could have a role in human neoplasia. Furthermore, in prostate cancer it has been demonstrated that TFF1 expression is closely associated with premalignant changes and neuroendocrine differentiation. In the present study, the expression of TFF1 was analysed in 18 human MTCs, comprising sporadic and familial tumours, C-cell hyperplasia, and one case of lymph gland metastasis. TFF1 expression was also examined in the cultures of a human MTC-derived tumour cell line (TT cell line). The results showed that ten sporadic tumours, three hereditary tumours (including C-cell hyperplasia), and one lymph gland metastasis displayed TFF1 immunoreactivity. Indirect fluorescence immunocytochemistry and Western blotting revealed that the TFF1 protein was strongly expressed in the TT cells. Northern analysis revealed that tumours and TT cells expressed the TFF1 transcript. Although the function of TFF1 protein in the carcinogenesis of MTC remains to be elucidated, its expression in the majority of cases of both sporadic and hereditary tumours, metastatic tumours, and in C-cell hyperplasia suggests that it may contribute to the pathogenesis of MTC.The Journal of Pathology 04/1998; 184(4):408-13. DOI:10.1002/(SICI)1096-9896(199804)184:4<408::AID-PATH1222>3.0.CO;2-3 · 7.33 Impact Factor