title: Immunolocalization of estrogen-producing and metabolizing enzymes in benign breast disease: comparison with normal breast and breast carcinoma.
abstract: It is well known that estrogens play important roles in the cell proliferation of breast carcinoma. Benign breast disease (BBD) contains a wide spectrum of diseases, and some are considered an important risk factor for subsequent breast carcinoma development. However, the significance of estrogens in BBD has remained largely unknown. Therefore, in this study, we examined tissue concentrations of estrogens and immunolocalization of estrogen-producing/metabolizing enzymes in BBD, and compared these findings with those in the normal breast and ductal carcinoma in situ (DCIS). Tissue concentration of estradiol in BBD (n = 9) was significantly (3.4-fold) higher than normal breast (n = 9) and nearly the same (0.7-fold) as in DCIS (n = 9). Immunoreactivity of estrogen sulfotransferase in BBD was significantly lower (n = 82) than normal breast (n = 28) but was not significantly different from DCIS (n = 28). Aromatase and steroid sulfatase immunoreactivities tended to be higher (P = 0.07) in BBD than in normal breast, and 17β-hydroxysteroid dehydrogenase type 1 immunoreactivity was significantly higher in BBD than normal breast in the postmenopausal tissues. Immunoreactivity of estrogen and progesterone receptors was also significantly higher in BBD than normal breast. These results suggest that tissue concentration of estradiol is increased in BBD at a level similar to DCIS, which is considered mainly due to loss of estrogen sulfotransferase expression. Increased local estradiol concentration in BBD due to aberrant expression of estrogen-producing/metabolizing enzymes may play important roles in the accumulation of estradiol-mediated growth and/or subsequent development of breast carcinoma.
authors.affiliation: Department of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Sasaki
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Miki
authors.forename: Hisashi
authors.initials: H
authors.lastname: Hirakawa
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Onodera
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Takagi
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Akahira
authors.forename: Seijiro
authors.initials: S
authors.lastname: Honma
authors.forename: Takanori
authors.initials: T
authors.lastname: Ishida
authors.forename: Mika
authors.initials: M
authors.lastname: Watanabe
authors.forename: Hironobu
authors.initials: H
authors.lastname: Sasano
authors.forename: Takashi
authors.initials: T
authors.lastname: Suzuki
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000032:analysis; D000328:Adult; D001141:Aromatase / Q000032:analysis; D001940:Breast / Q000201:enzymology*; D001941:Breast Diseases / Q000201:enzymology*; D001943:Breast Neoplasms / Q000201:enzymology*; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000201:enzymology; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D015238:Sulfotransferases / Q000032:analysis
chemical_list: D004967:Estrogens; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D015067:17-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D001141:Aromatase; D015238:Sulfotransferases; C020122:estrone sulfotransferase