Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status
Background Human 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) plays a vital role in steroidogenesis in breast tumors and may therefore be a suitable target for treatment of breast cancer. This study investigated the role of HSD3B1 in the pathogenesis of breast cancer in clinical and experimental...
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| Veröffentlicht in: | Annals of surgical oncology 2017-12, Vol.24 (13), p.4033-4041 |
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| creator | Chang, Yuan-Ching Chen, Chi-Kuan Chen, Ming-Jen Lin, Jiunn-Chang Lin, Chi-Hsin Huang, Wen-Chien Cheng, Shih-Ping Chen, Shan-Na Liu, Chien-Liang |
| description | Background
Human 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) plays a vital role in steroidogenesis in breast tumors and may therefore be a suitable target for treatment of breast cancer. This study investigated the role of HSD3B1 in the pathogenesis of breast cancer in clinical and experimental settings.
Methods
Expression of HSD3B1 in primary tumors of 258 breast cancer patients was evaluated by immunohistochemistry. Screening of breast cancer cell lines indicated that triple-negative MDA-MB-231 cells expressed HSD3B1. The effects from genetic and pharmacologic inhibition of HSD3B1 were assessed in vitro and in vivo.
Results
The findings showed that 44% of the 258 breast cancers were HSD3B1-positive. The HSD3B1-positivity was associated with advanced-stage disease (
p
= 0.009) and reduced recurrence-free survival (
p
= 0.048) but not with tumor subtype or estrogen receptor status. Silencing of HSD3B1 or treatment with an HSD3B1 inhibitor (trilostane) reduced colony formation in breast cancer cells. Knockdown of HSD3B1 inhibited cell proliferation and migration. Analysis of a murine xenograft tumor model indicated that trilostane significantly slowed tumor growth.
Conclusions
Expression of HSD3B1 in breast cancer is negatively associated with prognosis. The study found HSD3B1 to be a potential therapeutic target for breast cancer independent of estrogen receptor status. |
| doi_str_mv | 10.1245/s10434-017-6000-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1923744812</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1959546122</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-44e713a4475e6a2ac489afc69db9c5a4e60d6a777d58e00b867d4b433b76d4e33</originalsourceid><addsrcrecordid>eNp1kU1uFDEQhVuIiPzAAdggS2zYNPG_u5dhmJBIkYggrFtuuybpaMZuXG4lc4ucJQfhTLiZgBASG9uq-t4r26-qXjP6nnGpjpFRKWRNmak1pbTWz6oDpkpF6oY9L2eqm7rlWu1Xh4i3tICCqhfVPm-MlKblB9XD8n5MgDjEQOKKiB-P9dnWp3i_xQwpDp58hJu5cA3BIpCr7QiEkSGQDwksZrKwwUEiA5ITxOgGm8GTuyHfkMsYE7ksyhCxtM-DhxHKEvI8aYn5lyn5Ag7GXNCv2eYJX1Z7K7tGePW0H1XfTpdXi7P64vOn88XJRe2E4bmWEgwTtrxCgbbcOtm0duV06_vWKStBU6-tMcarBijtG2287KUQvdFeghBH1bud75ji9wkwd5sBHazXNkCcsGMtF-WTGsYL-vYf9DZOKZTbFUq1SmrGZ4rtKJciYoJVN6ZhY9O2Y7Sb4-p2cXUlhW6Oq9NF8-bJeeo34P8ofudTAL4DsLTCNaS_Rv_X9SeEyqHj</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1959546122</pqid></control><display><type>article</type><title>Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Chang, Yuan-Ching ; Chen, Chi-Kuan ; Chen, Ming-Jen ; Lin, Jiunn-Chang ; Lin, Chi-Hsin ; Huang, Wen-Chien ; Cheng, Shih-Ping ; Chen, Shan-Na ; Liu, Chien-Liang</creator><creatorcontrib>Chang, Yuan-Ching ; Chen, Chi-Kuan ; Chen, Ming-Jen ; Lin, Jiunn-Chang ; Lin, Chi-Hsin ; Huang, Wen-Chien ; Cheng, Shih-Ping ; Chen, Shan-Na ; Liu, Chien-Liang</creatorcontrib><description>Background
Human 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) plays a vital role in steroidogenesis in breast tumors and may therefore be a suitable target for treatment of breast cancer. This study investigated the role of HSD3B1 in the pathogenesis of breast cancer in clinical and experimental settings.
Methods
Expression of HSD3B1 in primary tumors of 258 breast cancer patients was evaluated by immunohistochemistry. Screening of breast cancer cell lines indicated that triple-negative MDA-MB-231 cells expressed HSD3B1. The effects from genetic and pharmacologic inhibition of HSD3B1 were assessed in vitro and in vivo.
Results
The findings showed that 44% of the 258 breast cancers were HSD3B1-positive. The HSD3B1-positivity was associated with advanced-stage disease (
p
= 0.009) and reduced recurrence-free survival (
p
= 0.048) but not with tumor subtype or estrogen receptor status. Silencing of HSD3B1 or treatment with an HSD3B1 inhibitor (trilostane) reduced colony formation in breast cancer cells. Knockdown of HSD3B1 inhibited cell proliferation and migration. Analysis of a murine xenograft tumor model indicated that trilostane significantly slowed tumor growth.
Conclusions
Expression of HSD3B1 in breast cancer is negatively associated with prognosis. The study found HSD3B1 to be a potential therapeutic target for breast cancer independent of estrogen receptor status.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-017-6000-6</identifier><identifier>PMID: 28744792</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Animals ; Biomarkers, Tumor - metabolism ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Carcinoma, Intraductal, Noninfiltrating - genetics ; Carcinoma, Intraductal, Noninfiltrating - metabolism ; Carcinoma, Intraductal, Noninfiltrating - pathology ; Cell Cycle ; Cell Movement ; Cell Proliferation ; Dehydrogenases ; Dihydrotestosterone - analogs & derivatives ; Dihydrotestosterone - pharmacology ; Estrogens ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Medical prognosis ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Multienzyme Complexes - antagonists & inhibitors ; Multienzyme Complexes - genetics ; Multienzyme Complexes - metabolism ; Oncology ; Progesterone Reductase - antagonists & inhibitors ; Progesterone Reductase - genetics ; Progesterone Reductase - metabolism ; Prognosis ; Receptors, Estrogen - metabolism ; RNA, Small Interfering - genetics ; Steroid Isomerases - antagonists & inhibitors ; Steroid Isomerases - genetics ; Steroid Isomerases - metabolism ; Steroidogenesis ; Surgery ; Surgical Oncology ; Survival Rate ; Translational Research and Biomarkers ; Tumor cell lines ; Tumor Cells, Cultured ; Tumors ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Annals of surgical oncology, 2017-12, Vol.24 (13), p.4033-4041</ispartof><rights>Society of Surgical Oncology 2017</rights><rights>Annals of Surgical Oncology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-44e713a4475e6a2ac489afc69db9c5a4e60d6a777d58e00b867d4b433b76d4e33</citedby><cites>FETCH-LOGICAL-c372t-44e713a4475e6a2ac489afc69db9c5a4e60d6a777d58e00b867d4b433b76d4e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-017-6000-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-017-6000-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28744792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Yuan-Ching</creatorcontrib><creatorcontrib>Chen, Chi-Kuan</creatorcontrib><creatorcontrib>Chen, Ming-Jen</creatorcontrib><creatorcontrib>Lin, Jiunn-Chang</creatorcontrib><creatorcontrib>Lin, Chi-Hsin</creatorcontrib><creatorcontrib>Huang, Wen-Chien</creatorcontrib><creatorcontrib>Cheng, Shih-Ping</creatorcontrib><creatorcontrib>Chen, Shan-Na</creatorcontrib><creatorcontrib>Liu, Chien-Liang</creatorcontrib><title>Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background
Human 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) plays a vital role in steroidogenesis in breast tumors and may therefore be a suitable target for treatment of breast cancer. This study investigated the role of HSD3B1 in the pathogenesis of breast cancer in clinical and experimental settings.
Methods
Expression of HSD3B1 in primary tumors of 258 breast cancer patients was evaluated by immunohistochemistry. Screening of breast cancer cell lines indicated that triple-negative MDA-MB-231 cells expressed HSD3B1. The effects from genetic and pharmacologic inhibition of HSD3B1 were assessed in vitro and in vivo.
Results
The findings showed that 44% of the 258 breast cancers were HSD3B1-positive. The HSD3B1-positivity was associated with advanced-stage disease (
p
= 0.009) and reduced recurrence-free survival (
p
= 0.048) but not with tumor subtype or estrogen receptor status. Silencing of HSD3B1 or treatment with an HSD3B1 inhibitor (trilostane) reduced colony formation in breast cancer cells. Knockdown of HSD3B1 inhibited cell proliferation and migration. Analysis of a murine xenograft tumor model indicated that trilostane significantly slowed tumor growth.
Conclusions
Expression of HSD3B1 in breast cancer is negatively associated with prognosis. The study found HSD3B1 to be a potential therapeutic target for breast cancer independent of estrogen receptor status.</description><subject>Animals</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Intraductal, Noninfiltrating - genetics</subject><subject>Carcinoma, Intraductal, Noninfiltrating - metabolism</subject><subject>Carcinoma, Intraductal, Noninfiltrating - pathology</subject><subject>Cell Cycle</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Dehydrogenases</subject><subject>Dihydrotestosterone - analogs & derivatives</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>Estrogens</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Multienzyme Complexes - antagonists & inhibitors</subject><subject>Multienzyme Complexes - genetics</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Oncology</subject><subject>Progesterone Reductase - antagonists & inhibitors</subject><subject>Progesterone Reductase - genetics</subject><subject>Progesterone Reductase - metabolism</subject><subject>Prognosis</subject><subject>Receptors, Estrogen - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>Steroid Isomerases - antagonists & inhibitors</subject><subject>Steroid Isomerases - genetics</subject><subject>Steroid Isomerases - metabolism</subject><subject>Steroidogenesis</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Survival Rate</subject><subject>Translational Research and Biomarkers</subject><subject>Tumor cell lines</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1uFDEQhVuIiPzAAdggS2zYNPG_u5dhmJBIkYggrFtuuybpaMZuXG4lc4ucJQfhTLiZgBASG9uq-t4r26-qXjP6nnGpjpFRKWRNmak1pbTWz6oDpkpF6oY9L2eqm7rlWu1Xh4i3tICCqhfVPm-MlKblB9XD8n5MgDjEQOKKiB-P9dnWp3i_xQwpDp58hJu5cA3BIpCr7QiEkSGQDwksZrKwwUEiA5ITxOgGm8GTuyHfkMsYE7ksyhCxtM-DhxHKEvI8aYn5lyn5Ag7GXNCv2eYJX1Z7K7tGePW0H1XfTpdXi7P64vOn88XJRe2E4bmWEgwTtrxCgbbcOtm0duV06_vWKStBU6-tMcarBijtG2287KUQvdFeghBH1bud75ji9wkwd5sBHazXNkCcsGMtF-WTGsYL-vYf9DZOKZTbFUq1SmrGZ4rtKJciYoJVN6ZhY9O2Y7Sb4-p2cXUlhW6Oq9NF8-bJeeo34P8ofudTAL4DsLTCNaS_Rv_X9SeEyqHj</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Chang, Yuan-Ching</creator><creator>Chen, Chi-Kuan</creator><creator>Chen, Ming-Jen</creator><creator>Lin, Jiunn-Chang</creator><creator>Lin, Chi-Hsin</creator><creator>Huang, Wen-Chien</creator><creator>Cheng, Shih-Ping</creator><creator>Chen, Shan-Na</creator><creator>Liu, Chien-Liang</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20171201</creationdate><title>Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status</title><author>Chang, Yuan-Ching ; Chen, Chi-Kuan ; Chen, Ming-Jen ; Lin, Jiunn-Chang ; Lin, Chi-Hsin ; Huang, Wen-Chien ; Cheng, Shih-Ping ; Chen, Shan-Na ; Liu, Chien-Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-44e713a4475e6a2ac489afc69db9c5a4e60d6a777d58e00b867d4b433b76d4e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Intraductal, Noninfiltrating - genetics</topic><topic>Carcinoma, Intraductal, Noninfiltrating - metabolism</topic><topic>Carcinoma, Intraductal, Noninfiltrating - pathology</topic><topic>Cell Cycle</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Dehydrogenases</topic><topic>Dihydrotestosterone - analogs & derivatives</topic><topic>Dihydrotestosterone - pharmacology</topic><topic>Estrogens</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Multienzyme Complexes - antagonists & inhibitors</topic><topic>Multienzyme Complexes - genetics</topic><topic>Multienzyme Complexes - metabolism</topic><topic>Oncology</topic><topic>Progesterone Reductase - antagonists & inhibitors</topic><topic>Progesterone Reductase - genetics</topic><topic>Progesterone Reductase - metabolism</topic><topic>Prognosis</topic><topic>Receptors, Estrogen - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>Steroid Isomerases - antagonists & inhibitors</topic><topic>Steroid Isomerases - genetics</topic><topic>Steroid Isomerases - metabolism</topic><topic>Steroidogenesis</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Survival Rate</topic><topic>Translational Research and Biomarkers</topic><topic>Tumor cell lines</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Yuan-Ching</creatorcontrib><creatorcontrib>Chen, Chi-Kuan</creatorcontrib><creatorcontrib>Chen, Ming-Jen</creatorcontrib><creatorcontrib>Lin, Jiunn-Chang</creatorcontrib><creatorcontrib>Lin, Chi-Hsin</creatorcontrib><creatorcontrib>Huang, Wen-Chien</creatorcontrib><creatorcontrib>Cheng, Shih-Ping</creatorcontrib><creatorcontrib>Chen, Shan-Na</creatorcontrib><creatorcontrib>Liu, Chien-Liang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Yuan-Ching</au><au>Chen, Chi-Kuan</au><au>Chen, Ming-Jen</au><au>Lin, Jiunn-Chang</au><au>Lin, Chi-Hsin</au><au>Huang, Wen-Chien</au><au>Cheng, Shih-Ping</au><au>Chen, Shan-Na</au><au>Liu, Chien-Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>24</volume><issue>13</issue><spage>4033</spage><epage>4041</epage><pages>4033-4041</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background
Human 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) plays a vital role in steroidogenesis in breast tumors and may therefore be a suitable target for treatment of breast cancer. This study investigated the role of HSD3B1 in the pathogenesis of breast cancer in clinical and experimental settings.
Methods
Expression of HSD3B1 in primary tumors of 258 breast cancer patients was evaluated by immunohistochemistry. Screening of breast cancer cell lines indicated that triple-negative MDA-MB-231 cells expressed HSD3B1. The effects from genetic and pharmacologic inhibition of HSD3B1 were assessed in vitro and in vivo.
Results
The findings showed that 44% of the 258 breast cancers were HSD3B1-positive. The HSD3B1-positivity was associated with advanced-stage disease (
p
= 0.009) and reduced recurrence-free survival (
p
= 0.048) but not with tumor subtype or estrogen receptor status. Silencing of HSD3B1 or treatment with an HSD3B1 inhibitor (trilostane) reduced colony formation in breast cancer cells. Knockdown of HSD3B1 inhibited cell proliferation and migration. Analysis of a murine xenograft tumor model indicated that trilostane significantly slowed tumor growth.
Conclusions
Expression of HSD3B1 in breast cancer is negatively associated with prognosis. The study found HSD3B1 to be a potential therapeutic target for breast cancer independent of estrogen receptor status.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>28744792</pmid><doi>10.1245/s10434-017-6000-6</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1068-9265 |
| ispartof | Annals of surgical oncology, 2017-12, Vol.24 (13), p.4033-4041 |
| issn | 1068-9265 1534-4681 |
| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Biomarkers, Tumor - metabolism Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Intraductal, Noninfiltrating - genetics Carcinoma, Intraductal, Noninfiltrating - metabolism Carcinoma, Intraductal, Noninfiltrating - pathology Cell Cycle Cell Movement Cell Proliferation Dehydrogenases Dihydrotestosterone - analogs & derivatives Dihydrotestosterone - pharmacology Estrogens Female Follow-Up Studies Humans Immunohistochemistry Medical prognosis Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Middle Aged Multienzyme Complexes - antagonists & inhibitors Multienzyme Complexes - genetics Multienzyme Complexes - metabolism Oncology Progesterone Reductase - antagonists & inhibitors Progesterone Reductase - genetics Progesterone Reductase - metabolism Prognosis Receptors, Estrogen - metabolism RNA, Small Interfering - genetics Steroid Isomerases - antagonists & inhibitors Steroid Isomerases - genetics Steroid Isomerases - metabolism Steroidogenesis Surgery Surgical Oncology Survival Rate Translational Research and Biomarkers Tumor cell lines Tumor Cells, Cultured Tumors Xenograft Model Antitumor Assays Xenografts |
| title | Expression of 3β-Hydroxysteroid Dehydrogenase Type 1 in Breast Cancer is Associated with Poor Prognosis Independent of Estrogen Receptor Status |
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