Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers
Purpose: Prostatic dihydrotestosterone (DHT) concentration is regulated by precursors from systemic circulation and prostatic enzymes of androgen metabolism, particularly 5α-reductases (i.e., SRD5A1 and SRD5A2). Therefore, the levels of expression SRD5A1 and SRD5A2 and the antiprostatic cancer growt...
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| Veröffentlicht in: | Clinical cancer research 2006-07, Vol.12 (13), p.4072-4079 |
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| creator | Xu, Yi Dalrymple, Susan L Becker, Robyn E Denmeade, Samuel R Isaacs, John T |
| description | Purpose: Prostatic dihydrotestosterone (DHT) concentration is regulated by precursors from systemic circulation and prostatic enzymes
of androgen metabolism, particularly 5α-reductases (i.e., SRD5A1 and SRD5A2). Therefore, the levels of expression SRD5A1 and
SRD5A2 and the antiprostatic cancer growth response to finasteride, a selective SRD5A2 inhibitor, versus the dual SRD5A1 and
SRD5A2 inhibitor, dutasteride, were compared.
Experimental Design: Real-time PCR and enzymatic assays were used to determine the levels of SRD5A1 and SRD5A2 in normal versus malignant rat
and human prostatic tissues. Rats bearing the Dunning R-3327H rat prostate cancer and nude mice bearing LNCaP or PC-3 human
prostate cancer xenografts were used as model systems. Tissue levels of testosterone and DHT were determined using liquid
chromatography-mass spectrometry.
Results: Prostate cancer cells express undetectable to low levels of SRD5A2 but elevated levels of SRD5A1 activity compared with nonmalignant
prostatic tissue. Daily oral treatment of rats with the SRD5A2 selective inhibitor, finasteride, reduces prostate weight and
DHT content but did not inhibit R-3327H rat prostate cancer growth or DHT content in intact (i.e., noncastrated) male rats.
In contrast, daily oral treatment with even a low 1 mg/kg/d dose of the dual SRD5A1 and SRD5A2 inhibitor, dutasteride, reduces
both normal prostate and H tumor DHT content and weight in intact rats while elevating tissue testosterone. Daily oral treatment
with finasteride significantly ( P < 0.05) inhibits growth of LNCaP human prostate cancer xenografts in intact male nude mice, but this inhibition is not as
great as that by equimolar oral dosing with dutasteride. This anticancer efficacy is not equivalent, however, to that produced
by castration. Only combination of dutasteride and castration produces a greater tumor inhibition ( P < 0.05) than castration monotherapy against androgen-responsive LNCaP cancers. In contrast, no response was induced by dutasteride
in nude mice bearing androgen-independent PC-3 human prostatic cancer xenografts.
Conclusions: These results document that testosterone is not as potent as DHT but does stimulate prostate cancer growth, thus combining
castration with dutasteride enhances therapeutic efficacy. |
| doi_str_mv | 10.1158/1078-0432.CCR-06-0184 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68602330</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68602330</sourcerecordid><originalsourceid>FETCH-LOGICAL-c407t-c5de67be155872b1969aa39a91d4673abcbd31f05339c7acf8b47a82d75154cd3</originalsourceid><addsrcrecordid>eNpFkMlOwzAQhi0EYn8EkE9IHAKeOF5yhFAWCQmEgKs1cZzGqG3AToX69ji0iNPM4ftn-Qg5AXYBIPQlMKUzVvD8oqpeMiYzBrrYIvsghMp4LsV26v-YPXIQ4wdjUAArdskeSA1aMbVP3p87DHO0_ayfekuvMfpI2z7QoXN0suhwYV1DJ23rLdoV7Vt6sxwwDi74xlGcol_EgT6HPg44pAHVGAjxiOy0OIvueFMPydvt5LW6zx6f7h6qq8fMFkwNmRWNk6p26Wit8hpKWSLyEktoCqk41rZuOLRMcF5ahbbVdaFQ540SIArb8ENytp77GfqvpYuDmfto3WyGC9cvo5FaspxzlkCxBm06NQbXms_g5xhWBpgZhZpRlhllmSTUMGlGoSl3ulmwrOeu-U9tDCbgfA10ftp9--CM_VUQXHQYbGcgN8BNejfnP99Wf78</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68602330</pqid></control><display><type>article</type><title>Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Xu, Yi ; Dalrymple, Susan L ; Becker, Robyn E ; Denmeade, Samuel R ; Isaacs, John T</creator><creatorcontrib>Xu, Yi ; Dalrymple, Susan L ; Becker, Robyn E ; Denmeade, Samuel R ; Isaacs, John T</creatorcontrib><description>Purpose: Prostatic dihydrotestosterone (DHT) concentration is regulated by precursors from systemic circulation and prostatic enzymes
of androgen metabolism, particularly 5α-reductases (i.e., SRD5A1 and SRD5A2). Therefore, the levels of expression SRD5A1 and
SRD5A2 and the antiprostatic cancer growth response to finasteride, a selective SRD5A2 inhibitor, versus the dual SRD5A1 and
SRD5A2 inhibitor, dutasteride, were compared.
Experimental Design: Real-time PCR and enzymatic assays were used to determine the levels of SRD5A1 and SRD5A2 in normal versus malignant rat
and human prostatic tissues. Rats bearing the Dunning R-3327H rat prostate cancer and nude mice bearing LNCaP or PC-3 human
prostate cancer xenografts were used as model systems. Tissue levels of testosterone and DHT were determined using liquid
chromatography-mass spectrometry.
Results: Prostate cancer cells express undetectable to low levels of SRD5A2 but elevated levels of SRD5A1 activity compared with nonmalignant
prostatic tissue. Daily oral treatment of rats with the SRD5A2 selective inhibitor, finasteride, reduces prostate weight and
DHT content but did not inhibit R-3327H rat prostate cancer growth or DHT content in intact (i.e., noncastrated) male rats.
In contrast, daily oral treatment with even a low 1 mg/kg/d dose of the dual SRD5A1 and SRD5A2 inhibitor, dutasteride, reduces
both normal prostate and H tumor DHT content and weight in intact rats while elevating tissue testosterone. Daily oral treatment
with finasteride significantly ( P < 0.05) inhibits growth of LNCaP human prostate cancer xenografts in intact male nude mice, but this inhibition is not as
great as that by equimolar oral dosing with dutasteride. This anticancer efficacy is not equivalent, however, to that produced
by castration. Only combination of dutasteride and castration produces a greater tumor inhibition ( P < 0.05) than castration monotherapy against androgen-responsive LNCaP cancers. In contrast, no response was induced by dutasteride
in nude mice bearing androgen-independent PC-3 human prostatic cancer xenografts.
Conclusions: These results document that testosterone is not as potent as DHT but does stimulate prostate cancer growth, thus combining
castration with dutasteride enhances therapeutic efficacy.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-06-0184</identifier><identifier>PMID: 16818707</identifier><language>eng</language><publisher>United States: American Association for Cancer Research</publisher><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - genetics ; 5-alpha Reductase Inhibitors ; 5α-reductase inhibitors ; Administration, Oral ; Animals ; Azasteroids - chemistry ; Azasteroids - pharmacology ; Azasteroids - therapeutic use ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chromatography, Liquid - methods ; Dihydrotestosterone - administration & dosage ; Dihydrotestosterone - chemistry ; Dihydrotestosterone - pharmacology ; Disease Models, Animal ; Dutasteride ; Enzyme Activation - drug effects ; Enzyme Inhibitors - administration & dosage ; Enzyme Inhibitors - chemistry ; Enzyme Inhibitors - pharmacology ; Finasteride - administration & dosage ; Finasteride - chemistry ; Finasteride - pharmacology ; Gene Expression Profiling ; Humans ; Male ; Mass Spectrometry - methods ; Mice ; Mice, Nude ; Molecular Conformation ; prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; Protein Isoforms - antagonists & inhibitors ; Protein Isoforms - genetics ; Rats ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - antagonists & inhibitors ; RNA, Messenger - genetics ; Structure-Activity Relationship ; Xenograft Model Antitumor Assays</subject><ispartof>Clinical cancer research, 2006-07, Vol.12 (13), p.4072-4079</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-c5de67be155872b1969aa39a91d4673abcbd31f05339c7acf8b47a82d75154cd3</citedby><cites>FETCH-LOGICAL-c407t-c5de67be155872b1969aa39a91d4673abcbd31f05339c7acf8b47a82d75154cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16818707$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Yi</creatorcontrib><creatorcontrib>Dalrymple, Susan L</creatorcontrib><creatorcontrib>Becker, Robyn E</creatorcontrib><creatorcontrib>Denmeade, Samuel R</creatorcontrib><creatorcontrib>Isaacs, John T</creatorcontrib><title>Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Prostatic dihydrotestosterone (DHT) concentration is regulated by precursors from systemic circulation and prostatic enzymes
of androgen metabolism, particularly 5α-reductases (i.e., SRD5A1 and SRD5A2). Therefore, the levels of expression SRD5A1 and
SRD5A2 and the antiprostatic cancer growth response to finasteride, a selective SRD5A2 inhibitor, versus the dual SRD5A1 and
SRD5A2 inhibitor, dutasteride, were compared.
Experimental Design: Real-time PCR and enzymatic assays were used to determine the levels of SRD5A1 and SRD5A2 in normal versus malignant rat
and human prostatic tissues. Rats bearing the Dunning R-3327H rat prostate cancer and nude mice bearing LNCaP or PC-3 human
prostate cancer xenografts were used as model systems. Tissue levels of testosterone and DHT were determined using liquid
chromatography-mass spectrometry.
Results: Prostate cancer cells express undetectable to low levels of SRD5A2 but elevated levels of SRD5A1 activity compared with nonmalignant
prostatic tissue. Daily oral treatment of rats with the SRD5A2 selective inhibitor, finasteride, reduces prostate weight and
DHT content but did not inhibit R-3327H rat prostate cancer growth or DHT content in intact (i.e., noncastrated) male rats.
In contrast, daily oral treatment with even a low 1 mg/kg/d dose of the dual SRD5A1 and SRD5A2 inhibitor, dutasteride, reduces
both normal prostate and H tumor DHT content and weight in intact rats while elevating tissue testosterone. Daily oral treatment
with finasteride significantly ( P < 0.05) inhibits growth of LNCaP human prostate cancer xenografts in intact male nude mice, but this inhibition is not as
great as that by equimolar oral dosing with dutasteride. This anticancer efficacy is not equivalent, however, to that produced
by castration. Only combination of dutasteride and castration produces a greater tumor inhibition ( P < 0.05) than castration monotherapy against androgen-responsive LNCaP cancers. In contrast, no response was induced by dutasteride
in nude mice bearing androgen-independent PC-3 human prostatic cancer xenografts.
Conclusions: These results document that testosterone is not as potent as DHT but does stimulate prostate cancer growth, thus combining
castration with dutasteride enhances therapeutic efficacy.</description><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - genetics</subject><subject>5-alpha Reductase Inhibitors</subject><subject>5α-reductase inhibitors</subject><subject>Administration, Oral</subject><subject>Animals</subject><subject>Azasteroids - chemistry</subject><subject>Azasteroids - pharmacology</subject><subject>Azasteroids - therapeutic use</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromatography, Liquid - methods</subject><subject>Dihydrotestosterone - administration & dosage</subject><subject>Dihydrotestosterone - chemistry</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Dutasteride</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Inhibitors - administration & dosage</subject><subject>Enzyme Inhibitors - chemistry</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Finasteride - administration & dosage</subject><subject>Finasteride - chemistry</subject><subject>Finasteride - pharmacology</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Male</subject><subject>Mass Spectrometry - methods</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular Conformation</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Protein Isoforms - antagonists & inhibitors</subject><subject>Protein Isoforms - genetics</subject><subject>Rats</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - antagonists & inhibitors</subject><subject>RNA, Messenger - genetics</subject><subject>Structure-Activity Relationship</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMlOwzAQhi0EYn8EkE9IHAKeOF5yhFAWCQmEgKs1cZzGqG3AToX69ji0iNPM4ftn-Qg5AXYBIPQlMKUzVvD8oqpeMiYzBrrYIvsghMp4LsV26v-YPXIQ4wdjUAArdskeSA1aMbVP3p87DHO0_ayfekuvMfpI2z7QoXN0suhwYV1DJ23rLdoV7Vt6sxwwDi74xlGcol_EgT6HPg44pAHVGAjxiOy0OIvueFMPydvt5LW6zx6f7h6qq8fMFkwNmRWNk6p26Wit8hpKWSLyEktoCqk41rZuOLRMcF5ahbbVdaFQ540SIArb8ENytp77GfqvpYuDmfto3WyGC9cvo5FaspxzlkCxBm06NQbXms_g5xhWBpgZhZpRlhllmSTUMGlGoSl3ulmwrOeu-U9tDCbgfA10ftp9--CM_VUQXHQYbGcgN8BNejfnP99Wf78</recordid><startdate>20060701</startdate><enddate>20060701</enddate><creator>Xu, Yi</creator><creator>Dalrymple, Susan L</creator><creator>Becker, Robyn E</creator><creator>Denmeade, Samuel R</creator><creator>Isaacs, John T</creator><general>American Association for Cancer Research</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>7X8</scope></search><sort><creationdate>20060701</creationdate><title>Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers</title><author>Xu, Yi ; Dalrymple, Susan L ; Becker, Robyn E ; Denmeade, Samuel R ; Isaacs, John T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-c5de67be155872b1969aa39a91d4673abcbd31f05339c7acf8b47a82d75154cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - genetics</topic><topic>5-alpha Reductase Inhibitors</topic><topic>5α-reductase inhibitors</topic><topic>Administration, Oral</topic><topic>Animals</topic><topic>Azasteroids - chemistry</topic><topic>Azasteroids - pharmacology</topic><topic>Azasteroids - therapeutic use</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromatography, Liquid - methods</topic><topic>Dihydrotestosterone - administration & dosage</topic><topic>Dihydrotestosterone - chemistry</topic><topic>Dihydrotestosterone - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Dutasteride</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Inhibitors - administration & dosage</topic><topic>Enzyme Inhibitors - chemistry</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Finasteride - administration & dosage</topic><topic>Finasteride - chemistry</topic><topic>Finasteride - pharmacology</topic><topic>Gene Expression Profiling</topic><topic>Humans</topic><topic>Male</topic><topic>Mass Spectrometry - methods</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Molecular Conformation</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Protein Isoforms - antagonists & inhibitors</topic><topic>Protein Isoforms - genetics</topic><topic>Rats</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - antagonists & inhibitors</topic><topic>RNA, Messenger - genetics</topic><topic>Structure-Activity Relationship</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Yi</creatorcontrib><creatorcontrib>Dalrymple, Susan L</creatorcontrib><creatorcontrib>Becker, Robyn E</creatorcontrib><creatorcontrib>Denmeade, Samuel R</creatorcontrib><creatorcontrib>Isaacs, John T</creatorcontrib><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>Xu, Yi</au><au>Dalrymple, Susan L</au><au>Becker, Robyn E</au><au>Denmeade, Samuel R</au><au>Isaacs, John T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2006-07-01</date><risdate>2006</risdate><volume>12</volume><issue>13</issue><spage>4072</spage><epage>4079</epage><pages>4072-4079</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Prostatic dihydrotestosterone (DHT) concentration is regulated by precursors from systemic circulation and prostatic enzymes
of androgen metabolism, particularly 5α-reductases (i.e., SRD5A1 and SRD5A2). Therefore, the levels of expression SRD5A1 and
SRD5A2 and the antiprostatic cancer growth response to finasteride, a selective SRD5A2 inhibitor, versus the dual SRD5A1 and
SRD5A2 inhibitor, dutasteride, were compared.
Experimental Design: Real-time PCR and enzymatic assays were used to determine the levels of SRD5A1 and SRD5A2 in normal versus malignant rat
and human prostatic tissues. Rats bearing the Dunning R-3327H rat prostate cancer and nude mice bearing LNCaP or PC-3 human
prostate cancer xenografts were used as model systems. Tissue levels of testosterone and DHT were determined using liquid
chromatography-mass spectrometry.
Results: Prostate cancer cells express undetectable to low levels of SRD5A2 but elevated levels of SRD5A1 activity compared with nonmalignant
prostatic tissue. Daily oral treatment of rats with the SRD5A2 selective inhibitor, finasteride, reduces prostate weight and
DHT content but did not inhibit R-3327H rat prostate cancer growth or DHT content in intact (i.e., noncastrated) male rats.
In contrast, daily oral treatment with even a low 1 mg/kg/d dose of the dual SRD5A1 and SRD5A2 inhibitor, dutasteride, reduces
both normal prostate and H tumor DHT content and weight in intact rats while elevating tissue testosterone. Daily oral treatment
with finasteride significantly ( P < 0.05) inhibits growth of LNCaP human prostate cancer xenografts in intact male nude mice, but this inhibition is not as
great as that by equimolar oral dosing with dutasteride. This anticancer efficacy is not equivalent, however, to that produced
by castration. Only combination of dutasteride and castration produces a greater tumor inhibition ( P < 0.05) than castration monotherapy against androgen-responsive LNCaP cancers. In contrast, no response was induced by dutasteride
in nude mice bearing androgen-independent PC-3 human prostatic cancer xenografts.
Conclusions: These results document that testosterone is not as potent as DHT but does stimulate prostate cancer growth, thus combining
castration with dutasteride enhances therapeutic efficacy.</abstract><cop>United States</cop><pub>American Association for Cancer Research</pub><pmid>16818707</pmid><doi>10.1158/1078-0432.CCR-06-0184</doi><tpages>8</tpages></addata></record> |
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| ispartof | Clinical cancer research, 2006-07, Vol.12 (13), p.4072-4079 |
| 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 | 3-Oxo-5-alpha-Steroid 4-Dehydrogenase - genetics 5-alpha Reductase Inhibitors 5α-reductase inhibitors Administration, Oral Animals Azasteroids - chemistry Azasteroids - pharmacology Azasteroids - therapeutic use Cell Line, Tumor Cell Proliferation - drug effects Chromatography, Liquid - methods Dihydrotestosterone - administration & dosage Dihydrotestosterone - chemistry Dihydrotestosterone - pharmacology Disease Models, Animal Dutasteride Enzyme Activation - drug effects Enzyme Inhibitors - administration & dosage Enzyme Inhibitors - chemistry Enzyme Inhibitors - pharmacology Finasteride - administration & dosage Finasteride - chemistry Finasteride - pharmacology Gene Expression Profiling Humans Male Mass Spectrometry - methods Mice Mice, Nude Molecular Conformation prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - metabolism Protein Isoforms - antagonists & inhibitors Protein Isoforms - genetics Rats Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - antagonists & inhibitors RNA, Messenger - genetics Structure-Activity Relationship Xenograft Model Antitumor Assays |
| title | Pharmacologic Basis for the Enhanced Efficacy of Dutasteride against Prostatic Cancers |
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