In vivo gene therapy with p53 or p21 adenovirus for prostate cancer
We introduced the gene for wild-type human p53 or p21, a critical downstream mediator of p53-induced growth suppression, into a p53-deficient mouse prostate cancer cell line using a recombinant adenoviral vector (Ad5CMV-p53 or Ad5CMV-p21). Elevated levels of endogenous mouse p21 mRNA provided eviden...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1995-11, Vol.55 (22), p.5151-5155 |
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| creator | EASTHMAN, J. A HALL, S. J THOMPSON, T. C SEHGAL, I WANG, J TIMME, T. L YANG, G CONNELL-CROWLEY, L ELLEDGE, S. J ZHANG, W.-W HARPER, J. W |
| description | We introduced the gene for wild-type human p53 or p21, a critical downstream mediator of p53-induced growth suppression, into a p53-deficient mouse prostate cancer cell line using a recombinant adenoviral vector (Ad5CMV-p53 or Ad5CMV-p21). Elevated levels of endogenous mouse p21 mRNA provided evidence for the functional activity of virally transduced p53. Functional activity of viral-transduced p21 was demonstrated through immunoprecipitation of cellular protein extracts, which showed that the viral-transduced p21 associates with cyclin-dependent kinase 2 and was sufficient to down-regulate the activity of the cyclin-dependent kinase by approximately 65%. In vitro growth assays revealed significantly higher growth suppression after Ad5CMV-p21 infection compared to Ad5CMV-p53. In vivo studies in syngeneic male mice with established s.c. prostate tumors demonstrated that the rate of growth and final tumor volume were reduced to a much greater extent in mice that received intratumor injection of Ad5CMV-p21 compared to Ad5CMV-p53. In addition, the survival of host animals bearing tumors that were infected with Ad5CMV-p21, but not Ad5CMV-p53, was significantly extended. These data suggest that Ad5CMV-p21 may be effective as a therapeutic agent for prostate cancer. |
| format | Article |
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A ; HALL, S. J ; THOMPSON, T. C ; SEHGAL, I ; WANG, J ; TIMME, T. L ; YANG, G ; CONNELL-CROWLEY, L ; ELLEDGE, S. J ; ZHANG, W.-W ; HARPER, J. W</creator><creatorcontrib>EASTHMAN, J. A ; HALL, S. J ; THOMPSON, T. C ; SEHGAL, I ; WANG, J ; TIMME, T. L ; YANG, G ; CONNELL-CROWLEY, L ; ELLEDGE, S. J ; ZHANG, W.-W ; HARPER, J. W</creatorcontrib><description>We introduced the gene for wild-type human p53 or p21, a critical downstream mediator of p53-induced growth suppression, into a p53-deficient mouse prostate cancer cell line using a recombinant adenoviral vector (Ad5CMV-p53 or Ad5CMV-p21). Elevated levels of endogenous mouse p21 mRNA provided evidence for the functional activity of virally transduced p53. Functional activity of viral-transduced p21 was demonstrated through immunoprecipitation of cellular protein extracts, which showed that the viral-transduced p21 associates with cyclin-dependent kinase 2 and was sufficient to down-regulate the activity of the cyclin-dependent kinase by approximately 65%. In vitro growth assays revealed significantly higher growth suppression after Ad5CMV-p21 infection compared to Ad5CMV-p53. In vivo studies in syngeneic male mice with established s.c. prostate tumors demonstrated that the rate of growth and final tumor volume were reduced to a much greater extent in mice that received intratumor injection of Ad5CMV-p21 compared to Ad5CMV-p53. In addition, the survival of host animals bearing tumors that were infected with Ad5CMV-p21, but not Ad5CMV-p53, was significantly extended. These data suggest that Ad5CMV-p21 may be effective as a therapeutic agent for prostate cancer.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 7585563</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenoviridae - genetics ; Animals ; Antineoplastic agents ; Biological and medical sciences ; Cell Division ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - genetics ; General aspects ; Genes, p53 ; Genetic Therapy ; Humans ; Male ; Medical sciences ; Mice ; Pharmacology. Drug treatments ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms - therapy ; Protein Kinase Inhibitors ; Tumor Cells, Cultured</subject><ispartof>Cancer research (Chicago, Ill.), 1995-11, Vol.55 (22), p.5151-5155</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2926151$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7585563$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>EASTHMAN, J. A</creatorcontrib><creatorcontrib>HALL, S. J</creatorcontrib><creatorcontrib>THOMPSON, T. 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Functional activity of viral-transduced p21 was demonstrated through immunoprecipitation of cellular protein extracts, which showed that the viral-transduced p21 associates with cyclin-dependent kinase 2 and was sufficient to down-regulate the activity of the cyclin-dependent kinase by approximately 65%. In vitro growth assays revealed significantly higher growth suppression after Ad5CMV-p21 infection compared to Ad5CMV-p53. In vivo studies in syngeneic male mice with established s.c. prostate tumors demonstrated that the rate of growth and final tumor volume were reduced to a much greater extent in mice that received intratumor injection of Ad5CMV-p21 compared to Ad5CMV-p53. In addition, the survival of host animals bearing tumors that were infected with Ad5CMV-p21, but not Ad5CMV-p53, was significantly extended. These data suggest that Ad5CMV-p21 may be effective as a therapeutic agent for prostate cancer.</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Division</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - genetics</subject><subject>General aspects</subject><subject>Genes, p53</subject><subject>Genetic Therapy</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Prostatic Neoplasms - therapy</topic><topic>Protein Kinase Inhibitors</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>EASTHMAN, J. A</creatorcontrib><creatorcontrib>HALL, S. J</creatorcontrib><creatorcontrib>THOMPSON, T. C</creatorcontrib><creatorcontrib>SEHGAL, I</creatorcontrib><creatorcontrib>WANG, J</creatorcontrib><creatorcontrib>TIMME, T. L</creatorcontrib><creatorcontrib>YANG, G</creatorcontrib><creatorcontrib>CONNELL-CROWLEY, L</creatorcontrib><creatorcontrib>ELLEDGE, S. J</creatorcontrib><creatorcontrib>ZHANG, W.-W</creatorcontrib><creatorcontrib>HARPER, J. W</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>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>EASTHMAN, J. A</au><au>HALL, S. J</au><au>THOMPSON, T. C</au><au>SEHGAL, I</au><au>WANG, J</au><au>TIMME, T. L</au><au>YANG, G</au><au>CONNELL-CROWLEY, L</au><au>ELLEDGE, S. J</au><au>ZHANG, W.-W</au><au>HARPER, J. W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo gene therapy with p53 or p21 adenovirus for prostate cancer</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1995-11-15</date><risdate>1995</risdate><volume>55</volume><issue>22</issue><spage>5151</spage><epage>5155</epage><pages>5151-5155</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>We introduced the gene for wild-type human p53 or p21, a critical downstream mediator of p53-induced growth suppression, into a p53-deficient mouse prostate cancer cell line using a recombinant adenoviral vector (Ad5CMV-p53 or Ad5CMV-p21). Elevated levels of endogenous mouse p21 mRNA provided evidence for the functional activity of virally transduced p53. Functional activity of viral-transduced p21 was demonstrated through immunoprecipitation of cellular protein extracts, which showed that the viral-transduced p21 associates with cyclin-dependent kinase 2 and was sufficient to down-regulate the activity of the cyclin-dependent kinase by approximately 65%. In vitro growth assays revealed significantly higher growth suppression after Ad5CMV-p21 infection compared to Ad5CMV-p53. In vivo studies in syngeneic male mice with established s.c. prostate tumors demonstrated that the rate of growth and final tumor volume were reduced to a much greater extent in mice that received intratumor injection of Ad5CMV-p21 compared to Ad5CMV-p53. In addition, the survival of host animals bearing tumors that were infected with Ad5CMV-p21, but not Ad5CMV-p53, was significantly extended. These data suggest that Ad5CMV-p21 may be effective as a therapeutic agent for prostate cancer.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>7585563</pmid><tpages>5</tpages></addata></record> |
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| subjects | Adenoviridae - genetics Animals Antineoplastic agents Biological and medical sciences Cell Division Cyclin-Dependent Kinase Inhibitor p21 Cyclins - genetics General aspects Genes, p53 Genetic Therapy Humans Male Medical sciences Mice Pharmacology. Drug treatments Prostatic Neoplasms - pathology Prostatic Neoplasms - therapy Protein Kinase Inhibitors Tumor Cells, Cultured |
| title | In vivo gene therapy with p53 or p21 adenovirus for prostate cancer |
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