Steroid Sulfatase and Estrogen Sulfotransferase in Human Endometrial Carcinoma
Purpose: Intratumoral metabolism and synthesis of estrogens are considered to play important roles in the pathogenesis and/or development of human endometrial carcinoma. Steroid sulfatase hydrolyzes biologically inactive estrogen sulfates to active estrogens, whereas estrogen sulfotransferase sulfon...
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| Veröffentlicht in: | Clinical cancer research 2004-09, Vol.10 (17), p.5850-5856 |
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| creator | UTSUNOMIYA, Hiroki ITO, Kiyoshi SUZUKI, Takashi KITAMURA, Takako KANEKO, Chika NAKATA, Taisuke NIIKURA, Hitoshi OKAMURA, Kunihiro YAEGASHI, Nobuo SASANO, Hironobu |
| description | Purpose: Intratumoral metabolism and synthesis of estrogens are considered to play important roles in the pathogenesis and/or development
of human endometrial carcinoma. Steroid sulfatase hydrolyzes biologically inactive estrogen sulfates to active estrogens,
whereas estrogen sulfotransferase sulfonates estrogens to estrogen sulfates. However, the status of steroid sulfatase and/or
estrogen sulfotransferase in human endometrial carcinoma has not been examined.
Experimental Design: We first examined the expression of steroid sulfatase and estrogen sulfotransferase in 6 normal endometrium and 76 endometrial
carcinoma using immunohistochemistry to elucidate the possible involvement of steroid sulfatase and estrogen sulfotransferase.
We then evaluated the enzymatic activity and the semiquantitative analysis of mRNA using reverse transcription-PCR in 21 endometrial
carcinomas. We correlated these findings with various clinicopathological parameters including the expression of aromatase,
17β-hydroxysteroid dehydrogenase type 1 and type 2.
Results: Steroid sulfatase and estrogen sulfotransferase immunoreactivity was detected in 65 of 76 (86%) and 22 of 76 (29%) cases,
respectively. Results of immunoreactivity for steroid sulfatase and estrogen sulfotransferase were significantly correlated
with those of enzymatic activity and semiquantitative analysis of mRNA. No significant correlations were detected among the
expression of the enzymes involved in intratumoral estrogen metabolism. There was a significant correlation between steroid
sulfatase/estrogen sulfotransferase ratio and clinical outcomes of the patients. However, there were no significant differences
between steroid sulfatase or estrogen sulfotransferase and estrogen receptor, progesterone receptor, Ki67, histologic grade,
or clinical outcomes of the patients.
Conclusions: Results of our study demonstrated that increased steroid sulfatase and decreased estrogen sulfotransferase expression in
human endometrial carcinomas may result in increased availability of biologically active estrogens and may be related to estrogen-dependent
biological features of carcinoma. |
| doi_str_mv | 10.1158/1078-0432.CCR-04-0040 |
| format | Article |
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of human endometrial carcinoma. Steroid sulfatase hydrolyzes biologically inactive estrogen sulfates to active estrogens,
whereas estrogen sulfotransferase sulfonates estrogens to estrogen sulfates. However, the status of steroid sulfatase and/or
estrogen sulfotransferase in human endometrial carcinoma has not been examined.
Experimental Design: We first examined the expression of steroid sulfatase and estrogen sulfotransferase in 6 normal endometrium and 76 endometrial
carcinoma using immunohistochemistry to elucidate the possible involvement of steroid sulfatase and estrogen sulfotransferase.
We then evaluated the enzymatic activity and the semiquantitative analysis of mRNA using reverse transcription-PCR in 21 endometrial
carcinomas. We correlated these findings with various clinicopathological parameters including the expression of aromatase,
17β-hydroxysteroid dehydrogenase type 1 and type 2.
Results: Steroid sulfatase and estrogen sulfotransferase immunoreactivity was detected in 65 of 76 (86%) and 22 of 76 (29%) cases,
respectively. Results of immunoreactivity for steroid sulfatase and estrogen sulfotransferase were significantly correlated
with those of enzymatic activity and semiquantitative analysis of mRNA. No significant correlations were detected among the
expression of the enzymes involved in intratumoral estrogen metabolism. There was a significant correlation between steroid
sulfatase/estrogen sulfotransferase ratio and clinical outcomes of the patients. However, there were no significant differences
between steroid sulfatase or estrogen sulfotransferase and estrogen receptor, progesterone receptor, Ki67, histologic grade,
or clinical outcomes of the patients.
Conclusions: Results of our study demonstrated that increased steroid sulfatase and decreased estrogen sulfotransferase expression in
human endometrial carcinomas may result in increased availability of biologically active estrogens and may be related to estrogen-dependent
biological features of carcinoma.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-04-0040</identifier><identifier>PMID: 15355916</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>17-Hydroxysteroid Dehydrogenases - genetics ; 17-Hydroxysteroid Dehydrogenases - metabolism ; Adenocarcinoma - enzymology ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Antineoplastic agents ; Aromatase - genetics ; Aromatase - metabolism ; Biological and medical sciences ; Carcinoma, Endometrioid - enzymology ; Carcinoma, Endometrioid - genetics ; Carcinoma, Endometrioid - pathology ; Endometrium - enzymology ; Endometrium - pathology ; Estrogens - metabolism ; Estrogens - pharmacology ; Female ; Humans ; Immunoenzyme Techniques ; Medical sciences ; Middle Aged ; Neoplasm Staging ; Neoplasms, Hormone-Dependent - enzymology ; Neoplasms, Hormone-Dependent - genetics ; Neoplasms, Hormone-Dependent - pathology ; Pharmacology. Drug treatments ; Prognosis ; Receptors, Estrogen - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Risk Factors ; RNA, Messenger - genetics ; Steryl-Sulfatase - genetics ; Steryl-Sulfatase - metabolism ; Sulfotransferases - genetics ; Sulfotransferases - metabolism ; Tumors</subject><ispartof>Clinical cancer research, 2004-09, Vol.10 (17), p.5850-5856</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-403cb52bc70e3c8a3cd2fa8b370c8ff917ac14a72ceb5e4120cee9411ae2ba673</citedby><cites>FETCH-LOGICAL-c487t-403cb52bc70e3c8a3cd2fa8b370c8ff917ac14a72ceb5e4120cee9411ae2ba673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,3345,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16097921$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15355916$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>UTSUNOMIYA, Hiroki</creatorcontrib><creatorcontrib>ITO, Kiyoshi</creatorcontrib><creatorcontrib>SUZUKI, Takashi</creatorcontrib><creatorcontrib>KITAMURA, Takako</creatorcontrib><creatorcontrib>KANEKO, Chika</creatorcontrib><creatorcontrib>NAKATA, Taisuke</creatorcontrib><creatorcontrib>NIIKURA, Hitoshi</creatorcontrib><creatorcontrib>OKAMURA, Kunihiro</creatorcontrib><creatorcontrib>YAEGASHI, Nobuo</creatorcontrib><creatorcontrib>SASANO, Hironobu</creatorcontrib><title>Steroid Sulfatase and Estrogen Sulfotransferase in Human Endometrial Carcinoma</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Intratumoral metabolism and synthesis of estrogens are considered to play important roles in the pathogenesis and/or development
of human endometrial carcinoma. Steroid sulfatase hydrolyzes biologically inactive estrogen sulfates to active estrogens,
whereas estrogen sulfotransferase sulfonates estrogens to estrogen sulfates. However, the status of steroid sulfatase and/or
estrogen sulfotransferase in human endometrial carcinoma has not been examined.
Experimental Design: We first examined the expression of steroid sulfatase and estrogen sulfotransferase in 6 normal endometrium and 76 endometrial
carcinoma using immunohistochemistry to elucidate the possible involvement of steroid sulfatase and estrogen sulfotransferase.
We then evaluated the enzymatic activity and the semiquantitative analysis of mRNA using reverse transcription-PCR in 21 endometrial
carcinomas. We correlated these findings with various clinicopathological parameters including the expression of aromatase,
17β-hydroxysteroid dehydrogenase type 1 and type 2.
Results: Steroid sulfatase and estrogen sulfotransferase immunoreactivity was detected in 65 of 76 (86%) and 22 of 76 (29%) cases,
respectively. Results of immunoreactivity for steroid sulfatase and estrogen sulfotransferase were significantly correlated
with those of enzymatic activity and semiquantitative analysis of mRNA. No significant correlations were detected among the
expression of the enzymes involved in intratumoral estrogen metabolism. There was a significant correlation between steroid
sulfatase/estrogen sulfotransferase ratio and clinical outcomes of the patients. However, there were no significant differences
between steroid sulfatase or estrogen sulfotransferase and estrogen receptor, progesterone receptor, Ki67, histologic grade,
or clinical outcomes of the patients.
Conclusions: Results of our study demonstrated that increased steroid sulfatase and decreased estrogen sulfotransferase expression in
human endometrial carcinomas may result in increased availability of biologically active estrogens and may be related to estrogen-dependent
biological features of carcinoma.</description><subject>17-Hydroxysteroid Dehydrogenases - genetics</subject><subject>17-Hydroxysteroid Dehydrogenases - metabolism</subject><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Antineoplastic agents</subject><subject>Aromatase - genetics</subject><subject>Aromatase - metabolism</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Endometrioid - enzymology</subject><subject>Carcinoma, Endometrioid - genetics</subject><subject>Carcinoma, Endometrioid - pathology</subject><subject>Endometrium - enzymology</subject><subject>Endometrium - pathology</subject><subject>Estrogens - metabolism</subject><subject>Estrogens - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Neoplasms, Hormone-Dependent - enzymology</subject><subject>Neoplasms, Hormone-Dependent - genetics</subject><subject>Neoplasms, Hormone-Dependent - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Prognosis</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Risk Factors</subject><subject>RNA, Messenger - genetics</subject><subject>Steryl-Sulfatase - genetics</subject><subject>Steryl-Sulfatase - metabolism</subject><subject>Sulfotransferases - genetics</subject><subject>Sulfotransferases - metabolism</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtr3DAQRkVpSDaXn9Dilxby4M3Ikiz7sZhNUlgayOVZjOVxVsWXVLIp_feRs1v2aT5mzozEYewLhzXnqrjhoIsUpMjWVfUYQwog4RNbcaV0KrJcfY75P3PGzkP4DcAlB3nKzrgSSpU8X7FfTxP50TXJ09y1OGGgBIcm2YTJj680fLTHyeMQWvLL1A3J_dzjkGyGZuxp8g67pEJv3TD2eMlOWuwCXR3qBXu53TxX9-n24e5n9WObWlnoKZUgbK2y2mogYQsUtslaLGqhwRZtW3KNlkvUmaVakeQZWKJSco6U1ZhrccG-7----fHPTGEyvQuWug4HGudg8rxQWpUQQbUHrR9D8NSaN-969P8MB7OINIsks0gyUWQMZhEZ974eHpjrnprj1sFcBL4dAAwWuzYqsi4cuRxKXWY8ctd7buded3-dJ2MjSd5ToGht9_EPbVShQLwDE-eKrA</recordid><startdate>20040901</startdate><enddate>20040901</enddate><creator>UTSUNOMIYA, Hiroki</creator><creator>ITO, Kiyoshi</creator><creator>SUZUKI, Takashi</creator><creator>KITAMURA, Takako</creator><creator>KANEKO, Chika</creator><creator>NAKATA, Taisuke</creator><creator>NIIKURA, Hitoshi</creator><creator>OKAMURA, Kunihiro</creator><creator>YAEGASHI, Nobuo</creator><creator>SASANO, Hironobu</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20040901</creationdate><title>Steroid Sulfatase and Estrogen Sulfotransferase in Human Endometrial Carcinoma</title><author>UTSUNOMIYA, Hiroki ; ITO, Kiyoshi ; SUZUKI, Takashi ; KITAMURA, Takako ; KANEKO, Chika ; NAKATA, Taisuke ; NIIKURA, Hitoshi ; OKAMURA, Kunihiro ; YAEGASHI, Nobuo ; SASANO, Hironobu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-403cb52bc70e3c8a3cd2fa8b370c8ff917ac14a72ceb5e4120cee9411ae2ba673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>17-Hydroxysteroid Dehydrogenases - genetics</topic><topic>17-Hydroxysteroid Dehydrogenases - metabolism</topic><topic>Adenocarcinoma - enzymology</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Antineoplastic agents</topic><topic>Aromatase - genetics</topic><topic>Aromatase - metabolism</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Endometrioid - enzymology</topic><topic>Carcinoma, Endometrioid - genetics</topic><topic>Carcinoma, Endometrioid - pathology</topic><topic>Endometrium - enzymology</topic><topic>Endometrium - pathology</topic><topic>Estrogens - metabolism</topic><topic>Estrogens - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>Neoplasms, Hormone-Dependent - enzymology</topic><topic>Neoplasms, Hormone-Dependent - genetics</topic><topic>Neoplasms, Hormone-Dependent - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Prognosis</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Risk Factors</topic><topic>RNA, Messenger - genetics</topic><topic>Steryl-Sulfatase - genetics</topic><topic>Steryl-Sulfatase - metabolism</topic><topic>Sulfotransferases - genetics</topic><topic>Sulfotransferases - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>UTSUNOMIYA, Hiroki</creatorcontrib><creatorcontrib>ITO, Kiyoshi</creatorcontrib><creatorcontrib>SUZUKI, Takashi</creatorcontrib><creatorcontrib>KITAMURA, Takako</creatorcontrib><creatorcontrib>KANEKO, Chika</creatorcontrib><creatorcontrib>NAKATA, Taisuke</creatorcontrib><creatorcontrib>NIIKURA, Hitoshi</creatorcontrib><creatorcontrib>OKAMURA, Kunihiro</creatorcontrib><creatorcontrib>YAEGASHI, Nobuo</creatorcontrib><creatorcontrib>SASANO, Hironobu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>UTSUNOMIYA, Hiroki</au><au>ITO, Kiyoshi</au><au>SUZUKI, Takashi</au><au>KITAMURA, Takako</au><au>KANEKO, Chika</au><au>NAKATA, Taisuke</au><au>NIIKURA, Hitoshi</au><au>OKAMURA, Kunihiro</au><au>YAEGASHI, Nobuo</au><au>SASANO, Hironobu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Steroid Sulfatase and Estrogen Sulfotransferase in Human Endometrial Carcinoma</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2004-09-01</date><risdate>2004</risdate><volume>10</volume><issue>17</issue><spage>5850</spage><epage>5856</epage><pages>5850-5856</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Intratumoral metabolism and synthesis of estrogens are considered to play important roles in the pathogenesis and/or development
of human endometrial carcinoma. Steroid sulfatase hydrolyzes biologically inactive estrogen sulfates to active estrogens,
whereas estrogen sulfotransferase sulfonates estrogens to estrogen sulfates. However, the status of steroid sulfatase and/or
estrogen sulfotransferase in human endometrial carcinoma has not been examined.
Experimental Design: We first examined the expression of steroid sulfatase and estrogen sulfotransferase in 6 normal endometrium and 76 endometrial
carcinoma using immunohistochemistry to elucidate the possible involvement of steroid sulfatase and estrogen sulfotransferase.
We then evaluated the enzymatic activity and the semiquantitative analysis of mRNA using reverse transcription-PCR in 21 endometrial
carcinomas. We correlated these findings with various clinicopathological parameters including the expression of aromatase,
17β-hydroxysteroid dehydrogenase type 1 and type 2.
Results: Steroid sulfatase and estrogen sulfotransferase immunoreactivity was detected in 65 of 76 (86%) and 22 of 76 (29%) cases,
respectively. Results of immunoreactivity for steroid sulfatase and estrogen sulfotransferase were significantly correlated
with those of enzymatic activity and semiquantitative analysis of mRNA. No significant correlations were detected among the
expression of the enzymes involved in intratumoral estrogen metabolism. There was a significant correlation between steroid
sulfatase/estrogen sulfotransferase ratio and clinical outcomes of the patients. However, there were no significant differences
between steroid sulfatase or estrogen sulfotransferase and estrogen receptor, progesterone receptor, Ki67, histologic grade,
or clinical outcomes of the patients.
Conclusions: Results of our study demonstrated that increased steroid sulfatase and decreased estrogen sulfotransferase expression in
human endometrial carcinomas may result in increased availability of biologically active estrogens and may be related to estrogen-dependent
biological features of carcinoma.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15355916</pmid><doi>10.1158/1078-0432.CCR-04-0040</doi><tpages>7</tpages></addata></record> |
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| ispartof | Clinical cancer research, 2004-09, Vol.10 (17), p.5850-5856 |
| issn | 1078-0432 1557-3265 |
| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 17-Hydroxysteroid Dehydrogenases - genetics 17-Hydroxysteroid Dehydrogenases - metabolism Adenocarcinoma - enzymology Adenocarcinoma - genetics Adenocarcinoma - pathology Antineoplastic agents Aromatase - genetics Aromatase - metabolism Biological and medical sciences Carcinoma, Endometrioid - enzymology Carcinoma, Endometrioid - genetics Carcinoma, Endometrioid - pathology Endometrium - enzymology Endometrium - pathology Estrogens - metabolism Estrogens - pharmacology Female Humans Immunoenzyme Techniques Medical sciences Middle Aged Neoplasm Staging Neoplasms, Hormone-Dependent - enzymology Neoplasms, Hormone-Dependent - genetics Neoplasms, Hormone-Dependent - pathology Pharmacology. Drug treatments Prognosis Receptors, Estrogen - metabolism Reverse Transcriptase Polymerase Chain Reaction Risk Factors RNA, Messenger - genetics Steryl-Sulfatase - genetics Steryl-Sulfatase - metabolism Sulfotransferases - genetics Sulfotransferases - metabolism Tumors |
| title | Steroid Sulfatase and Estrogen Sulfotransferase in Human Endometrial Carcinoma |
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