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Estrogen receptors (alpha and beta) and 17beta-hydroxysteroid dehydrogenase type 1 and 2 in thyroid disorders: possible in situ estrogen synthesis and actions.
Mod Pathol. 2003 May; 16(5):437-44.MP

Abstract

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) alpha and beta 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 ERalpha and beta 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 ERalpha and beta and 17beta-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. ERalpha labeling index, or percentage of cells immunopositive for ERalpha, 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 ERalpha in normal thyroid glands. In papillary carcinoma, ERalpha 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. ERbeta immunoreactivity was detected in both follicular and C-cells of normal thyroid glands, including those in developing fetal thyroid glands. In addition, ERbeta immunoreactivity was detected in the nuclei of various thyroid lesions. But no significant correlations were detected between ERbeta labeling index and clinicopathological findings including age, menopausal status, gender, and/or histological type of thyroid lesions. 17beta-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 ERalpha, may become more pronounced in neoplasms, particularly in papillary carcinoma arising in premenopausal women.

Authors+Show Affiliations

Department of Pathology, Tohoku University School of Medicine, Sendai, Japan. wakako@patholo2.med.tohoku.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12748250

Citation

Kawabata, Wakako, et al. "Estrogen Receptors (alpha and Beta) and 17beta-hydroxysteroid Dehydrogenase Type 1 and 2 in Thyroid Disorders: Possible in Situ Estrogen Synthesis and Actions." Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, vol. 16, no. 5, 2003, pp. 437-44.
Kawabata W, Suzuki T, Moriya T, et al. Estrogen receptors (alpha and beta) and 17beta-hydroxysteroid dehydrogenase type 1 and 2 in thyroid disorders: possible in situ estrogen synthesis and actions. Mod Pathol. 2003;16(5):437-44.
Kawabata, W., Suzuki, T., Moriya, T., Fujimori, K., Naganuma, H., Inoue, S., Kinouchi, Y., Kameyama, K., Takami, H., Shimosegawa, T., & Sasano, H. (2003). Estrogen receptors (alpha and beta) and 17beta-hydroxysteroid dehydrogenase type 1 and 2 in thyroid disorders: possible in situ estrogen synthesis and actions. Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 16(5), 437-44.
Kawabata W, et al. Estrogen Receptors (alpha and Beta) and 17beta-hydroxysteroid Dehydrogenase Type 1 and 2 in Thyroid Disorders: Possible in Situ Estrogen Synthesis and Actions. Mod Pathol. 2003;16(5):437-44. PubMed PMID: 12748250.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Estrogen receptors (alpha and beta) and 17beta-hydroxysteroid dehydrogenase type 1 and 2 in thyroid disorders: possible in situ estrogen synthesis and actions. AU - Kawabata,Wakako, AU - Suzuki,Takashi, AU - Moriya,Takuya, AU - Fujimori,Keisei, AU - Naganuma,Hiroshi, AU - Inoue,Satoshi, AU - Kinouchi,Yositaka, AU - Kameyama,Kaori, AU - Takami,Hiroshi, AU - Shimosegawa,Tooru, AU - Sasano,Hironobu, PY - 2003/5/16/pubmed PY - 2003/12/12/medline PY - 2003/5/16/entrez SP - 437 EP - 44 JF - Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc JO - Mod Pathol VL - 16 IS - 5 N2 - 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) alpha and beta 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 ERalpha and beta 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 ERalpha and beta and 17beta-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. ERalpha labeling index, or percentage of cells immunopositive for ERalpha, 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 ERalpha in normal thyroid glands. In papillary carcinoma, ERalpha 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. ERbeta immunoreactivity was detected in both follicular and C-cells of normal thyroid glands, including those in developing fetal thyroid glands. In addition, ERbeta immunoreactivity was detected in the nuclei of various thyroid lesions. But no significant correlations were detected between ERbeta labeling index and clinicopathological findings including age, menopausal status, gender, and/or histological type of thyroid lesions. 17beta-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 ERalpha, may become more pronounced in neoplasms, particularly in papillary carcinoma arising in premenopausal women. SN - 0893-3952 UR - https://www.unboundmedicine.com/medline/citation/12748250/Estrogen_receptors__alpha_and_beta__and_17beta_hydroxysteroid_dehydrogenase_type_1_and_2_in_thyroid_disorders:_possible_in_situ_estrogen_synthesis_and_actions_ L2 - https://doi.org/10.1097/01.MP.0000066800.44492.1B DB - PRIME DP - Unbound Medicine ER -