Steroid-converting enzymes in human ovarian carcinomas

Justin C. Chura; Hyung S. Ryu; Marc Simard; Donald Poirier; Yves Tremblay; Doris C. Brooker; Charles H. Blomquist; Peter A Argenta

doi:10.1016/j.mce.2008.07.015

Steroid-converting enzymes in human ovarian carcinomas

Justin C. Chura, Hyung S. Ryu, Marc Simard, Donald Poirier, Yves Tremblay, Doris C. Brooker, Charles H. Blomquist, Peter A Argenta

Obstetrics, Gynecology and Women's Health - Oncology

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

Anti-estrogen therapies for treating ovarian carcinoma have had mixed outcomes suggesting some tumors may be estrogen-dependent. We assayed the activity levels of 17β-hydroxysteroid dehydrogenase (17β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), 3α-hydroxysteroid dehydrogenase (3α-HSD/3-KSR) and estrone sulfatase in a series of ovarian epithelial carcinomas. 17β-HSD activity ratios with estradiol (E ₂ ) and testosterone (T), and inhibition by isoform-specific inhibitors were used to estimate the contributions of 17β-HSD isoforms. Activity levels were highest for estrone sulfatase, followed, respectively by 17β-HSD, 3α-HSD/3-KSR, and 3β-HSD. E ₂ /T activity ratios varied widely between samples. A 17β-HSD type 1 inhibition pattern was observed in 23% of the samples and a type 2 pattern in 25%. E ₂ formation from estrone sulfate (E ₁ S) was detected in 98% (47/48) of the samples. 17β-HSD type 1, type 2 and type 5 mRNA was detected in matched primary tumor and metastases. Evaluation of 17β-HSD and sulfatase activity levels, activity ratios and inhibition patterns may help predict tumor response to endocrine therapy.

Original language	English (US)
Pages (from-to)	51-58
Number of pages	8
Journal	Molecular and Cellular Endocrinology
Volume	301
Issue number	1-2
DOIs	https://doi.org/10.1016/j.mce.2008.07.015
State	Published - Mar 25 2009

Keywords

17β-Hydroxysteroid dehydrogenase
3α-Hydroxysteroid dehydrogenase
3β-Hydroxysteroid dehydrogenase
Estrone sulfatase
Ovarian cancer
Steroid metabolism

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title = "Steroid-converting enzymes in human ovarian carcinomas",

abstract = " Anti-estrogen therapies for treating ovarian carcinoma have had mixed outcomes suggesting some tumors may be estrogen-dependent. We assayed the activity levels of 17β-hydroxysteroid dehydrogenase (17β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), 3α-hydroxysteroid dehydrogenase (3α-HSD/3-KSR) and estrone sulfatase in a series of ovarian epithelial carcinomas. 17β-HSD activity ratios with estradiol (E 2 ) and testosterone (T), and inhibition by isoform-specific inhibitors were used to estimate the contributions of 17β-HSD isoforms. Activity levels were highest for estrone sulfatase, followed, respectively by 17β-HSD, 3α-HSD/3-KSR, and 3β-HSD. E 2 /T activity ratios varied widely between samples. A 17β-HSD type 1 inhibition pattern was observed in 23% of the samples and a type 2 pattern in 25%. E 2 formation from estrone sulfate (E 1 S) was detected in 98% (47/48) of the samples. 17β-HSD type 1, type 2 and type 5 mRNA was detected in matched primary tumor and metastases. Evaluation of 17β-HSD and sulfatase activity levels, activity ratios and inhibition patterns may help predict tumor response to endocrine therapy.",

keywords = "17β-Hydroxysteroid dehydrogenase, 3α-Hydroxysteroid dehydrogenase, 3β-Hydroxysteroid dehydrogenase, Estrone sulfatase, Ovarian cancer, Steroid metabolism",

author = "Chura, {Justin C.} and Ryu, {Hyung S.} and Marc Simard and Donald Poirier and Yves Tremblay and Brooker, {Doris C.} and Blomquist, {Charles H.} and Argenta, {Peter A}",

year = "2009",

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T1 - Steroid-converting enzymes in human ovarian carcinomas

AU - Chura, Justin C.

AU - Ryu, Hyung S.

AU - Simard, Marc

AU - Poirier, Donald

AU - Tremblay, Yves

AU - Brooker, Doris C.

AU - Blomquist, Charles H.

AU - Argenta, Peter A

PY - 2009/3/25

Y1 - 2009/3/25

N2 - Anti-estrogen therapies for treating ovarian carcinoma have had mixed outcomes suggesting some tumors may be estrogen-dependent. We assayed the activity levels of 17β-hydroxysteroid dehydrogenase (17β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), 3α-hydroxysteroid dehydrogenase (3α-HSD/3-KSR) and estrone sulfatase in a series of ovarian epithelial carcinomas. 17β-HSD activity ratios with estradiol (E 2 ) and testosterone (T), and inhibition by isoform-specific inhibitors were used to estimate the contributions of 17β-HSD isoforms. Activity levels were highest for estrone sulfatase, followed, respectively by 17β-HSD, 3α-HSD/3-KSR, and 3β-HSD. E 2 /T activity ratios varied widely between samples. A 17β-HSD type 1 inhibition pattern was observed in 23% of the samples and a type 2 pattern in 25%. E 2 formation from estrone sulfate (E 1 S) was detected in 98% (47/48) of the samples. 17β-HSD type 1, type 2 and type 5 mRNA was detected in matched primary tumor and metastases. Evaluation of 17β-HSD and sulfatase activity levels, activity ratios and inhibition patterns may help predict tumor response to endocrine therapy.

AB - Anti-estrogen therapies for treating ovarian carcinoma have had mixed outcomes suggesting some tumors may be estrogen-dependent. We assayed the activity levels of 17β-hydroxysteroid dehydrogenase (17β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), 3α-hydroxysteroid dehydrogenase (3α-HSD/3-KSR) and estrone sulfatase in a series of ovarian epithelial carcinomas. 17β-HSD activity ratios with estradiol (E 2 ) and testosterone (T), and inhibition by isoform-specific inhibitors were used to estimate the contributions of 17β-HSD isoforms. Activity levels were highest for estrone sulfatase, followed, respectively by 17β-HSD, 3α-HSD/3-KSR, and 3β-HSD. E 2 /T activity ratios varied widely between samples. A 17β-HSD type 1 inhibition pattern was observed in 23% of the samples and a type 2 pattern in 25%. E 2 formation from estrone sulfate (E 1 S) was detected in 98% (47/48) of the samples. 17β-HSD type 1, type 2 and type 5 mRNA was detected in matched primary tumor and metastases. Evaluation of 17β-HSD and sulfatase activity levels, activity ratios and inhibition patterns may help predict tumor response to endocrine therapy.

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KW - Steroid metabolism

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