AROMATASE AND 17-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1 IN HUMAN BREAST-CARCINOMA

Citation
H. Sasano et al., AROMATASE AND 17-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1 IN HUMAN BREAST-CARCINOMA, The Journal of clinical endocrinology and metabolism, 81(11), 1996, pp. 4042-4046
Citations number
21
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
81
Issue
11
Year of publication
1996
Pages
4042 - 4046
Database
ISI
SICI code
0021-972X(1996)81:11<4042:AA1DTI>2.0.ZU;2-8
Abstract
The in situ formation of estradiol plays an important role in the deve lopment and biological behavior of human breast cancer Aromatase and 1 7 beta-hydroxysteroid dehydrogenase type 1 (17 beta-HSD type 1) are tw o principal enzymes involved in in situ estradiol production. We evalu ated the expression of aromatase and 17 beta-HSD type 1 by immunohisto chemistry in 41 cases of invasive breast carcinoma (19 lobular and 22 ductal). We then examined the correlation among the expression of thes e enzymes, estrogen (ER) and progesterone (PR) receptor status, Ki67 l abeling index of carcinoma cells, age, and the clinical stage of the p atients. Marked aromatase immunoreactivity was observed in stromal cel ls around carcinomatous glands in 32 of 41 cases (78%), and 17 beta-HS D type 1 immunoreactivity was detected in carcinoma cells in 23 of 41 cases (56%). There was a significant correlation observed between expr ession of 17 beta-HSD type 1 and aromatase in invasive lobular carcino ma (P = 0.0119), but not in invasive ductal carcinoma. There was an in verse correlation between aromatase and ER status in invasive ductal c arcinoma (P = 0.0213), but not in invasive lobular carcinoma. No other correlations were observed among 17 beta-HSD type 1, aromatase, PR, E R, clinical stage, age, and Ki67 labeling indexes. Aromatase and 17 be ta-HSD are not always expressed simultaneously in human breast carcino ma, but their simultaneous expression is more frequent in invasive lob ular carcinoma than invasive ductal carcinoma. Consequently, different mechanisms may be involved in the regulation of expression of these t wo enzymes in human breast carcinoma.