title: Estrogen receptor expression in human pituitary: correlation with immunohistochemistry in normal tissue, and immunohistochemistry and morphology in macroadenomas.
abstract: Forty-one human pituitary adenoma specimens were examined for the presence of estrogen receptor (ER) messenger ribonucleic acid and protein using a combination of ribonuclease protection assay, [3H] estradiol ([3H]E2) binding, and ER immunohistochemistry. ER messenger ribonucleic acid prevalence was high in PRL-immunoreactive tumors (2 of 2), moderate in GH/PRL tumors (2 of 5), and low or absent (0 of 4) in GH tumors. In the GH/PRL-immunostaining tumors, the presence of the ER was uniformly associated with elevated serum PRL levels. Among the gonadotropin-immunostaining tumors, 10 of 17 were ER positive; within this group, those with gonadotroph adenoma characteristics were ER positive, whereas those with null cell/oncocytic characteristics were ER negative. Of the tumors that did not immunostain for any known anterior pituitary hormones, 3 of 11 were ER positive. ER immunohistochemistry in 14 tumors revealed a 100% correlation with ribonuclease protection assay results, whereas [3H]E2 binding, determined in 9 tumors, showed an 87% correlation. In summary, it appears that PRL and a specific class of gonadotropin-immunostaining tumors (identifiable by specific characteristics on electron microscope) contain ER, whereas GH-immunostaining tumors are ER negative. ER expression in normal pituitary paralleled that in macroadenomas (GH, 2.3%; PRL, 50%; FSH, 70%; LH, 83%; TSH, 4%; ACTH, 1%). The ER-positive tumors represent a subset whose growth and secretory profiles may be influenced by the gonadal steroidal milieu or by pharmacological agents that affect E2 levels or ER function.
authors.affiliation: Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
authors.forename: K E
authors.initials: KE
authors.lastname: Friend
authors.forename: Y K
authors.initials: YK
authors.lastname: Chiou
authors.forename: M B
authors.initials: MB
authors.lastname: Lopes
authors.forename: E R
authors.initials: ER
authors.lastname: Laws
authors.forename: K M
authors.initials: KM
authors.lastname: Hughes
authors.forename: M A
authors.initials: MA
authors.lastname: Shupnik
mesh_terms: D000236:Adenoma / Q000378:metabolism* / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000032:analysis; D004958:Estradiol / Q000378:metabolism; D005640:Follicle Stimulating Hormone / Q000032:analysis; D037201:Follicle Stimulating Hormone, beta Subunit; D015870:Gene Expression; D015292:Glycoprotein Hormones, alpha Subunit / Q000032:analysis; D013006:Growth Hormone / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007986:Luteinizing Hormone / Q000032:analysis; D010902:Pituitary Gland / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D010911:Pituitary Neoplasms / Q000378:metabolism* / Q000473:pathology; D011388:Prolactin / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000032:analysis / Q000096:biosynthesis*; D012016:Reference Values; D013972:Thyrotropin / Q000032:analysis
chemical_list: D037201:Follicle Stimulating Hormone, beta Subunit; D015292:Glycoprotein Hormones, alpha Subunit; D012333:RNA, Messenger; D011960:Receptors, Estrogen; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone