ESTROGEN-RECEPTOR EXPRESSION IN HUMAN PITUITARY - CORRELATION WITH IMMUNOHISTOCHEMISTRY IN NORMAL TISSUE, AND IMMUNOHISTOCHEMISTRY AND MORPHOLOGY IN MACROADENOMAS
Ke. Friend et al., ESTROGEN-RECEPTOR EXPRESSION IN HUMAN PITUITARY - CORRELATION WITH IMMUNOHISTOCHEMISTRY IN NORMAL TISSUE, AND IMMUNOHISTOCHEMISTRY AND MORPHOLOGY IN MACROADENOMAS, The Journal of clinical endocrinology and metabolism, 78(6), 1994, pp. 1497-1504
Forty-one human pituitary adenoma specimens were examined for the pres
ence of estrogen receptor (ER) messenger ribonucleic acid and protein
using a combination of ribonuclease protection assay, [H-3] estradiol
([H-3]E(2)) binding, and ER immunohistochemistry. ER messenger ribonuc
leic acid prevalence was high in PRL-immunoreactive tumors (2 of 2), m
oderate in GH/PRL tumors (2 of 5), and low or absent (0 of 4) in GH tu
mors. In the GH/PRL-immunostaining tumors, the presence of the ER was
uniformly associated with elevated serum PRL levels. Among the gonadot
ropin-immunostaining tumors, 10 of 17 were ER positive; within this gr
oup, those with gonadotroph adenoma characteristics were ER positive,
whereas those with null cell/oncocytic characteristics were ER negativ
e. Of the tumors that did not immunostain for any known anterior pitui
tary hormones, 3 of 11 were ER positive. ER immunohistochemistry in 14
tumors revealed a 100% correlation with ribonuclease protection assay
results, whereas [H-3]E(2) 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 chara
cteristics on electron microscope) contain ER, whereas GH-immunostaini
ng tumors are ER negative. ER expression in normal pituitary parallele
d 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 a
nd secretory profiles may be influenced by the gonadal steroidal milie
u or by pharmacological agents that affect E(2) levels or ER function.