title: Estrogen and progesterone receptor expression in postmenopausal tamoxifen-exposed endometrial pathologies.
abstract: Assessment of receptor levels in tamoxifen-exposed endometrial pathologies may indicate endometrial cells potential for interaction with tamoxifen. To assess this assumption, we analyzed estrogen receptor (ER) and progesterone receptor (PR) expression by an immunohistochemical technique in endometrial specimens with benign hyperplasia, benign polyps, and carcinoma obtained from postmenopausal breast cancer patients treated with tamoxifen (study group) and from age-matched healthy postmenopausal women treated with estrogen replacement therapy (control group I) and not treated with estrogen replacement therapy (control group II). Overall gland and stromal ER expression of benign endometrial hyperplasia and of benign endometrial polyps was significantly higher in control groups I and II than that obtained from the study group (endometrial hyperplasia: P = 0.0274 and 0.00093, respectively, and P = 0.00003 and 0.00001, respectively; benign endometrial polyps: P = 0.02889 and 0.00596, respectively; and P = 0.00228 and 0.00005, respectively), while there were no differences between the two control groups. Overall gland and stromal PR expression was nearly similar in all the three groups (P = NS). There was no correlation between the length of tamoxifen treatment and the presence of ER and PR in various endometrial pathologies in the tamoxifen-treated patients. The significantly lower ER expression in most benign endometrial pathologies obtained from postmenopausal tamoxifen treated patients may further support the weak estrogen-like effect of tamoxifen on the endometrium in the menopause.
authors.affiliation: Department of Obstetrics and Gynecology, Sapir Medical Center, Kfar Saba, Israel.
authors.forename: I
authors.initials: I
authors.lastname: Cohen
authors.forename: Y
authors.initials: Y
authors.lastname: Beyth
authors.forename: M M
authors.initials: MM
authors.lastname: Altaras
authors.forename: J
authors.initials: J
authors.lastname: Shapira
authors.forename: R
authors.initials: R
authors.lastname: Tepper
authors.forename: M
authors.initials: M
authors.lastname: Cardoba
authors.forename: D
authors.initials: D
authors.lastname: Yigael
authors.forename: A
authors.initials: A
authors.lastname: Figer
authors.forename: A
authors.initials: A
authors.lastname: Fishman
authors.forename: J
authors.initials: J
authors.lastname: Berenhein
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects* / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000097:blood / Q000188:drug therapy; D004714:Endometrial Hyperplasia / Q000097:blood / Q000139:chemically induced* / Q000473:pathology*; D016889:Endometrial Neoplasms / Q000097:blood / Q000139:chemically induced* / Q000648:ultrastructure*; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D011127:Polyps / Q000097:blood / Q000139:chemically induced* / Q000648:ultrastructure*; D017698:Postmenopause / Q000502:physiology*; D011960:Receptors, Estrogen / Q000096:biosynthesis*; D011980:Receptors, Progesterone / Q000096:biosynthesis*; D017154:Stromal Cells / Q000187:drug effects / Q000648:ultrastructure; D013629:Tamoxifen / Q000009:adverse effects* / Q000627:therapeutic use
chemical_list: D018931:Antineoplastic Agents, Hormonal; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013629:Tamoxifen; D004958:Estradiol