Both epidemiological and experimental findings suggest the possible roles of sex steroids in the pathogenesis and/or development of various human thyroid disorders. In this study, we evaluated the expression of estrogen receptors (ER) ␣ and  in normal thyroid glands (N ؍ 25; female: n ؍ 13, male: n ؍ 10, unknown: n ؍ 2) ranging in age from fetus to adult. Furthermore, using immunohistochemistry, we investigated the expression of ER␣ and  in 206 cases of thyroid disorders, including 24 adenomatous goiters, 23 follicular adenomas, and 159 thyroid carcinomas. In addition, we also studied the mRNA expression of ER␣ and  and 17-hydroxysteroid dehydrogenase Type 1 and 2, enzymes involved in the interconversion between estrone and estradiol, using reverse transcription polymerase chain reaction (RT-PCR), in 48 of these 206 cases (10 adenomatous goiters, 10 follicular adenomas, and 28 papillary thyroid carcinomas) in which fresh frozen tissues were available for examination to further elucidate the possible involvement of intracrine estrogen metabolism and/or actions in thyroid disorders. ER␣ labeling index, or percentage of cells immunopositive for ER␣, was significantly higher in adenomatous goiter (14.2 ؎ 6.4), follicular adenoma (13.4 ؎ 5.1), and thyroid carcinoma (16.4 ؎ 2.1) than in normal thyroid gland (0; P < .05). Few follicular cells were positive for ER␣ in normal thyroid glands. In papillary carcinoma, ER␣ labeling index was significantly higher in premenopausal women (28.1 ؎ 4.5) than in postmenopausal women (14.2 ؎ 2.9) and in men of various ages (7.6 ؎ 2.7; P < .05). In other histological types of thyroid carcinoma, no significant correlations were detected. ER immunoreactivity was detected in both follicular and C-cells of normal thyroid glands, including those in developing fetal thyroid glands. In addition, ER immunoreactivity was detected in the nuclei of various thyroid lesions. But no significant correlations were detected between ER labeling index and clinicopathological findings including age, menopausal status, gender, and/or histological type of thyroid lesions. 17-hydroxysteroid dehydrogenase Type 1 expression was detected in 31/48 (64.0%) of the cases examined, whereas Type 2 was detected only in 3/46 (6.3%) of all the cases examined. These results demonstrated that estrogens may influence the development, physiology, and pathology of human thyroid glands, and these effects, especially through ER␣, may become more pronounced in neoplasms, particularly in papillary carcinoma arising in premenopausal women. Biological effects of estrogens are generally mediated through an initial interaction with the estrogen receptor (ER), a member of the superfamily of nuclear receptors. Identification of ER is an initial step in understanding the estrogenic effects on various
EBAG9 has been recently identified as an oestrogen responsive gene in MCF-7 human breast carcinoma cells. EBAG9 is identical to RCAS1, a cancer cell surface antigen possibly involved in immune escape. In this study, we examined the expression of EBAG9/RCAS1 in human breast carcinomas using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). EBAG9 immunoreactivity was also associated with various clinicopathological parameters, including intratumoural infiltration of inflammatory cells, to examine the biological significance of EBAG9 in human breast carcinomas. EBAG9 immunoreactivity was detected in the entire surface and cytoplasm of carcinoma cells in 82 out of 91 invasive ductal carcinomas (90.1%). In non-neoplastic mammary glands, EBAG9 immunoreactivity was weakly present on the luminal surface of epithelial cells. Results from RT-PCR (n = 7) were consistent with those of immunohistochemistry. EBAG9 immunoreactivity was significantly associated with estrogen receptor (ER) α labelling index (P = 0.0081), and inversely associated with the degree of intratumoural infiltration of mononuclear cells (P = 0.0020), or CD3+ T lymphocytes (P = 0.0025). This study suggests that EBAG9 is produced via ER in carcinoma cells and inhibits the intratumoural infiltration of T lymphocytes in the context of a possible endocrine–immune interaction in human breast carcinomas. © 2001 Cancer Research Campaign http://www.bjcancer.com
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