Starving the Addiction: New Opportunities for Durable Suppression of AR Signaling in Prostate Cancer
Clinical data and models of human disease indicate that androgen receptor (AR) activity is essential for prostate cancer development, growth, and progression. The dependence of prostatic adenocarcinoma on AR signaling at all stages of disease has thereby been exploited in the treatment of disseminat...
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| Veröffentlicht in: | Clinical cancer research 2009-08, Vol.15 (15), p.4792-4798 |
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| container_title | Clinical cancer research |
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| creator | KNUDSEN, Karen E SCHER, Howard I |
| description | Clinical data and models of human disease indicate that androgen receptor (AR) activity is essential for prostate cancer development,
growth, and progression. The dependence of prostatic adenocarcinoma on AR signaling at all stages of disease has thereby been
exploited in the treatment of disseminated tumors, for which ablation of AR function is the goal of first-line therapy. Although
these strategies are initially effective, recurrent tumors arise with restored AR activity, and no durable treatment has yet
been identified to combat this stage of disease. New insights into AR regulation and the mechanisms underlying resurgent AR
activity have provided fertile ground for the development of novel strategies to more effectively inhibit receptor activity
and prolong the transition to therapeutic failure. |
| doi_str_mv | 10.1158/1078-0432.CCR-08-2660 |
| format | Article |
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growth, and progression. The dependence of prostatic adenocarcinoma on AR signaling at all stages of disease has thereby been
exploited in the treatment of disseminated tumors, for which ablation of AR function is the goal of first-line therapy. Although
these strategies are initially effective, recurrent tumors arise with restored AR activity, and no durable treatment has yet
been identified to combat this stage of disease. New insights into AR regulation and the mechanisms underlying resurgent AR
activity have provided fertile ground for the development of novel strategies to more effectively inhibit receptor activity
and prolong the transition to therapeutic failure.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-08-2660</identifier><identifier>PMID: 19638458</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Androgen Antagonists - therapeutic use ; Androgen Receptor Antagonists ; Androgens - metabolism ; Anilides - therapeutic use ; Antineoplastic agents ; Biological and medical sciences ; Flutamide - therapeutic use ; Gynecology. Andrology. Obstetrics ; Humans ; Male ; Male genital diseases ; Medical sciences ; Nephrology. Urinary tract diseases ; Nitriles - therapeutic use ; Pharmacology. Drug treatments ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; Protein Structure, Tertiary - physiology ; Receptors, Androgen - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Tosyl Compounds - therapeutic use ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Clinical cancer research, 2009-08, Vol.15 (15), p.4792-4798</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-ea76e9ad11963ba2444beb8e28a40220919cbfdad8030d227badd2c7023b5cb43</citedby><cites>FETCH-LOGICAL-c540t-ea76e9ad11963ba2444beb8e28a40220919cbfdad8030d227badd2c7023b5cb43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21879460$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19638458$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KNUDSEN, Karen E</creatorcontrib><creatorcontrib>SCHER, Howard I</creatorcontrib><title>Starving the Addiction: New Opportunities for Durable Suppression of AR Signaling in Prostate Cancer</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Clinical data and models of human disease indicate that androgen receptor (AR) activity is essential for prostate cancer development,
growth, and progression. The dependence of prostatic adenocarcinoma on AR signaling at all stages of disease has thereby been
exploited in the treatment of disseminated tumors, for which ablation of AR function is the goal of first-line therapy. Although
these strategies are initially effective, recurrent tumors arise with restored AR activity, and no durable treatment has yet
been identified to combat this stage of disease. New insights into AR regulation and the mechanisms underlying resurgent AR
activity have provided fertile ground for the development of novel strategies to more effectively inhibit receptor activity
and prolong the transition to therapeutic failure.</description><subject>Androgen Antagonists - therapeutic use</subject><subject>Androgen Receptor Antagonists</subject><subject>Androgens - metabolism</subject><subject>Anilides - therapeutic use</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Flutamide - therapeutic use</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nitriles - therapeutic use</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Protein Structure, Tertiary - physiology</subject><subject>Receptors, Androgen - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Tosyl Compounds - therapeutic use</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkVtv1DAQhSMEoqXwE0B-QYiHFF8ThwekVbhKFUVdeLYce7Ixysap7bTi3-N0lwKSpbHkb45nzimK5wSfEyLkG4JrWWLO6HnbXpVYlrSq8IPilAhRl4xW4mG-_2FOiicx_sSYcIL54-KENBWTXMjTwm6TDjdu2qE0ANpY60xyfnqLvsItupxnH9IyueQgot4H9H4JuhsBbZd5DhBjRpHv0eYKbd1u0uMq5Cb0LfiYdALU6slAeFo86vUY4dmxnhU_Pn743n4uLy4_fWk3F6URHKcSdF1Boy1Zx-s05Zx30EmgUnNMKW5IY7reaisxw5bSutPWUlNjyjphOs7OincH3Xnp9mANTCnoUc3B7XX4pbx26v-XyQ1q528UlZwSIrPAq6NA8NcLxKT2LhoYRz2BX6KqGROsqWSTSXEgTV41BujvfyFYrQGp1Xy1mq9yQApLtQaU-178O-LfrmMiGXh5BHQ0euxDdtDFe44SWTf8Tuj1gRvcbrh1AZS58zqnAjqYQRGxHl43lP0GaSGpbA</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>KNUDSEN, Karen E</creator><creator>SCHER, Howard I</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><scope>5PM</scope></search><sort><creationdate>20090801</creationdate><title>Starving the Addiction: New Opportunities for Durable Suppression of AR Signaling in Prostate Cancer</title><author>KNUDSEN, Karen E ; SCHER, Howard I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-ea76e9ad11963ba2444beb8e28a40220919cbfdad8030d227badd2c7023b5cb43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Androgen Antagonists - therapeutic use</topic><topic>Androgen Receptor Antagonists</topic><topic>Androgens - metabolism</topic><topic>Anilides - therapeutic use</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Flutamide - therapeutic use</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nitriles - therapeutic use</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Protein Structure, Tertiary - physiology</topic><topic>Receptors, Androgen - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Tosyl Compounds - therapeutic use</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KNUDSEN, Karen E</creatorcontrib><creatorcontrib>SCHER, Howard I</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KNUDSEN, Karen E</au><au>SCHER, Howard I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Starving the Addiction: New Opportunities for Durable Suppression of AR Signaling in Prostate Cancer</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2009-08-01</date><risdate>2009</risdate><volume>15</volume><issue>15</issue><spage>4792</spage><epage>4798</epage><pages>4792-4798</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Clinical data and models of human disease indicate that androgen receptor (AR) activity is essential for prostate cancer development,
growth, and progression. The dependence of prostatic adenocarcinoma on AR signaling at all stages of disease has thereby been
exploited in the treatment of disseminated tumors, for which ablation of AR function is the goal of first-line therapy. Although
these strategies are initially effective, recurrent tumors arise with restored AR activity, and no durable treatment has yet
been identified to combat this stage of disease. New insights into AR regulation and the mechanisms underlying resurgent AR
activity have provided fertile ground for the development of novel strategies to more effectively inhibit receptor activity
and prolong the transition to therapeutic failure.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>19638458</pmid><doi>10.1158/1078-0432.CCR-08-2660</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Androgen Antagonists - therapeutic use Androgen Receptor Antagonists Androgens - metabolism Anilides - therapeutic use Antineoplastic agents Biological and medical sciences Flutamide - therapeutic use Gynecology. Andrology. Obstetrics Humans Male Male genital diseases Medical sciences Nephrology. Urinary tract diseases Nitriles - therapeutic use Pharmacology. Drug treatments Prostatic Neoplasms - drug therapy Prostatic Neoplasms - metabolism Protein Structure, Tertiary - physiology Receptors, Androgen - metabolism Signal Transduction - drug effects Signal Transduction - physiology Tosyl Compounds - therapeutic use Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Starving the Addiction: New Opportunities for Durable Suppression of AR Signaling in Prostate Cancer |
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