Androgen receptor action in hormone-dependent and recurrent prostate cancer
The importance of androgens and androgen receptors (AR) in primary prostate cancer is well established. Metastatic disease is usually treated with some form of androgen ablation, which is effective for a limited amount of time. The role of AR in prostate cancers that recur despite androgen ablation...
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Veröffentlicht in: | Journal of cellular biochemistry 2006-10, Vol.99 (2), p.362-372 |
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description | The importance of androgens and androgen receptors (AR) in primary prostate cancer is well established. Metastatic disease is usually treated with some form of androgen ablation, which is effective for a limited amount of time. The role of AR in prostate cancers that recur despite androgen ablation therapy is less certain. Most of these tumors express prostate specific antigen (PSA), an androgen‐regulated gene; moreover, AR is generally highly expressed in recurrent prostate cancer. We propose that AR continues to play a role in many of these tumors and that it is not only the levels of AR, ligands, and co‐regulators, but also the changes in cell signaling that induce AR action in recurrent prostate cancer. These pathways are, therefore, potential therapeutic targets. J. Cell. Biochem. 99: 362–372, 2006. © 2006 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/jcb.20811 |
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Metastatic disease is usually treated with some form of androgen ablation, which is effective for a limited amount of time. The role of AR in prostate cancers that recur despite androgen ablation therapy is less certain. Most of these tumors express prostate specific antigen (PSA), an androgen‐regulated gene; moreover, AR is generally highly expressed in recurrent prostate cancer. We propose that AR continues to play a role in many of these tumors and that it is not only the levels of AR, ligands, and co‐regulators, but also the changes in cell signaling that induce AR action in recurrent prostate cancer. These pathways are, therefore, potential therapeutic targets. J. Cell. Biochem. 99: 362–372, 2006. © 2006 Wiley‐Liss, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.20811</identifier><identifier>PMID: 16619264</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>androgen receptor ; Androgens - metabolism ; Animals ; Cell Proliferation ; cell signaling ; co-activator ; Gene Expression ; Humans ; Male ; Models, Biological ; Mutation ; Neoplasm Recurrence, Local - genetics ; Neoplasm Recurrence, Local - metabolism ; Neoplasm Recurrence, Local - pathology ; Neoplasms, Hormone-Dependent - genetics ; Neoplasms, Hormone-Dependent - metabolism ; Neoplasms, Hormone-Dependent - pathology ; prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Receptors, Androgen - chemistry ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Signal Transduction</subject><ispartof>Journal of cellular biochemistry, 2006-10, Vol.99 (2), p.362-372</ispartof><rights>Copyright © 2006 Wiley‐Liss, Inc.</rights><rights>Copyright 2006 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4271-6e8fd6c1663e1cf2e5d037193ad7b3d95560aa08bf102336b4b6a9d5c55bda543</citedby><cites>FETCH-LOGICAL-c4271-6e8fd6c1663e1cf2e5d037193ad7b3d95560aa08bf102336b4b6a9d5c55bda543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.20811$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.20811$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16619264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Agoulnik, Irina U.</creatorcontrib><creatorcontrib>Weigel, Nancy L.</creatorcontrib><title>Androgen receptor action in hormone-dependent and recurrent prostate cancer</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>The importance of androgens and androgen receptors (AR) in primary prostate cancer is well established. Metastatic disease is usually treated with some form of androgen ablation, which is effective for a limited amount of time. The role of AR in prostate cancers that recur despite androgen ablation therapy is less certain. Most of these tumors express prostate specific antigen (PSA), an androgen‐regulated gene; moreover, AR is generally highly expressed in recurrent prostate cancer. We propose that AR continues to play a role in many of these tumors and that it is not only the levels of AR, ligands, and co‐regulators, but also the changes in cell signaling that induce AR action in recurrent prostate cancer. These pathways are, therefore, potential therapeutic targets. J. Cell. Biochem. 99: 362–372, 2006. © 2006 Wiley‐Liss, Inc.</description><subject>androgen receptor</subject><subject>Androgens - metabolism</subject><subject>Animals</subject><subject>Cell Proliferation</subject><subject>cell signaling</subject><subject>co-activator</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Male</subject><subject>Models, Biological</subject><subject>Mutation</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Neoplasm Recurrence, Local - metabolism</subject><subject>Neoplasm Recurrence, Local - pathology</subject><subject>Neoplasms, Hormone-Dependent - genetics</subject><subject>Neoplasms, Hormone-Dependent - metabolism</subject><subject>Neoplasms, Hormone-Dependent - pathology</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, Androgen - chemistry</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Signal Transduction</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAQRS0EouWx4AdQVkgs0voR2_GyVFDeLACxtBx7AimtU-xEwN-T0gIrVqORzj0zuggdEDwgGNPh1BYDinNCNlCfYCXTTGTZJupjyXBKGaE9tBPjFGOsFKPbqEeEIIqKrI-uRt6F-hl8EsDCoqlDYmxT1T6pfPJSh3ntIXWwAO_AN4nxbgm2ISy3RahjYxpIrPEWwh7aKs0swv567qLHs9OH8Xl6fTe5GI-uU5tRSVIBeemE7X5gQGxJgTvMJFHMOFkwpzgX2BicFyXBlDFRZIUwynHLeeEMz9guOlp5u_tvLcRGz6toYTYzHuo2apHnNJeYd-DxCrTdozFAqRehmpvwqQnWy-Z015z-bq5jD9fStpiD-yPXVXXAcAW8VzP4_N-kL8cnP8p0lahiAx-_CRNetZBMcv10O9H3T5fiRmVKS_YFMyOG4w</recordid><startdate>20061001</startdate><enddate>20061001</enddate><creator>Agoulnik, Irina U.</creator><creator>Weigel, Nancy L.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</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>20061001</creationdate><title>Androgen receptor action in hormone-dependent and recurrent prostate cancer</title><author>Agoulnik, Irina U. ; Weigel, Nancy L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4271-6e8fd6c1663e1cf2e5d037193ad7b3d95560aa08bf102336b4b6a9d5c55bda543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>androgen receptor</topic><topic>Androgens - metabolism</topic><topic>Animals</topic><topic>Cell Proliferation</topic><topic>cell signaling</topic><topic>co-activator</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Male</topic><topic>Models, Biological</topic><topic>Mutation</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Neoplasm Recurrence, Local - metabolism</topic><topic>Neoplasm Recurrence, Local - pathology</topic><topic>Neoplasms, Hormone-Dependent - genetics</topic><topic>Neoplasms, Hormone-Dependent - metabolism</topic><topic>Neoplasms, Hormone-Dependent - pathology</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Receptors, Androgen - chemistry</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Agoulnik, Irina U.</creatorcontrib><creatorcontrib>Weigel, Nancy L.</creatorcontrib><collection>Istex</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>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Agoulnik, Irina U.</au><au>Weigel, Nancy L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Androgen receptor action in hormone-dependent and recurrent prostate cancer</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2006-10-01</date><risdate>2006</risdate><volume>99</volume><issue>2</issue><spage>362</spage><epage>372</epage><pages>362-372</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>The importance of androgens and androgen receptors (AR) in primary prostate cancer is well established. Metastatic disease is usually treated with some form of androgen ablation, which is effective for a limited amount of time. The role of AR in prostate cancers that recur despite androgen ablation therapy is less certain. Most of these tumors express prostate specific antigen (PSA), an androgen‐regulated gene; moreover, AR is generally highly expressed in recurrent prostate cancer. We propose that AR continues to play a role in many of these tumors and that it is not only the levels of AR, ligands, and co‐regulators, but also the changes in cell signaling that induce AR action in recurrent prostate cancer. These pathways are, therefore, potential therapeutic targets. J. Cell. Biochem. 99: 362–372, 2006. © 2006 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>16619264</pmid><doi>10.1002/jcb.20811</doi><tpages>11</tpages></addata></record> |
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subjects | androgen receptor Androgens - metabolism Animals Cell Proliferation cell signaling co-activator Gene Expression Humans Male Models, Biological Mutation Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - metabolism Neoplasm Recurrence, Local - pathology Neoplasms, Hormone-Dependent - genetics Neoplasms, Hormone-Dependent - metabolism Neoplasms, Hormone-Dependent - pathology prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Receptors, Androgen - chemistry Receptors, Androgen - genetics Receptors, Androgen - metabolism Signal Transduction |
title | Androgen receptor action in hormone-dependent and recurrent prostate cancer |
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