Double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus in combination with radiotherapy elicits an enhanced anti-tumor effect
Radiation therapy, a mainstay for anti-tumor therapeutic regimens for a variety of tumor types, triggers tumor cell apoptotic pathways by either directly eliciting DNA damage or indirectly inducing the formation of oxygen radicals. In an effort to augment radiation therapy, we generated a double E1B...
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Veröffentlicht in: | Gene therapy 2009-09, Vol.16 (9), p.1111-1121 |
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description | Radiation therapy, a mainstay for anti-tumor therapeutic regimens for a variety of tumor types, triggers tumor cell apoptotic pathways by either directly eliciting DNA damage or indirectly inducing the formation of oxygen radicals. In an effort to augment radiation therapy, we generated a double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus (Ad−ΔE1B19/55). In combination with radiotherapy, greater cytotoxicity was observed for Ad−ΔE1B19/55 than for the single E1B 55 kDa-deleted oncolytic Ad (Ad−ΔE1B55). Consistent with this observation, higher levels of p53, phospho-p53, phospho-Chk1, phospho-Chk2, PI3K (phosphatidylinositol-3-kinase), phospho-AKT, cytochrome c, and cleavage of PARP (poly (ADP-ribose) polymerase) and caspase-3 were observed in cells treated with Ad−ΔE1B19/55 compared with those treated with Ad−ΔE1B55, indicating that the E1B 19 kDa present in Ad−ΔE1B55 may partially block radiation-induced apoptosis. A significant therapeutic benefit was also observed
in vivo
when oncolytic Ads and radiation were combined. Tumors treated with Ad−ΔE1B19/55 and radiation showed large areas of necrosis and apoptosis with the corresponding induction of p53. Finally, consistent with
in vitro
observations, the combination of Ad−ΔE1B19/55 and radiation was more efficacious than the combination of Ad−ΔE1B55 and radiation. Taken together, these results present a strong therapeutic rationale for combining radiation therapy with E1B 19 kDa-deleted oncolytic Ad. |
doi_str_mv | 10.1038/gt.2009.72 |
format | Article |
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in vivo
when oncolytic Ads and radiation were combined. Tumors treated with Ad−ΔE1B19/55 and radiation showed large areas of necrosis and apoptosis with the corresponding induction of p53. Finally, consistent with
in vitro
observations, the combination of Ad−ΔE1B19/55 and radiation was more efficacious than the combination of Ad−ΔE1B55 and radiation. Taken together, these results present a strong therapeutic rationale for combining radiation therapy with E1B 19 kDa-deleted oncolytic Ad.</description><identifier>ISSN: 0969-7128</identifier><identifier>EISSN: 1476-5462</identifier><identifier>DOI: 10.1038/gt.2009.72</identifier><identifier>PMID: 19494843</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adenoviridae - genetics ; Adenovirus E1B Proteins - genetics ; Adenoviruses ; Ageing, cell death ; AKT protein ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Apoptosis ; Apoptosis - genetics ; Applied cell therapy and gene therapy ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Biotechnology ; Cancer ; Care and treatment ; Caspase-3 ; Cell Biology ; Cell physiology ; CHK1 protein ; Combined Modality Therapy ; Cytochrome c ; Cytotoxicity ; DNA damage ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; Gene Therapy ; Genetic aspects ; Genetic vectors ; Health. Pharmaceutical industry ; Human Genetics ; Humans ; Industrial applications and implications. Economical aspects ; Male ; Medical sciences ; Methods ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Molecular and cellular biology ; Nanotechnology ; Oncolysis ; Oncolytic Virotherapy - methods ; Oncolytic Viruses - genetics ; original-article ; p53 Protein ; Patient outcomes ; Poly(ADP-ribose) polymerase ; Radiation therapy ; Radiotherapy ; Ribose ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy ; Tumors ; Uterine Cervical Neoplasms - pathology ; Uterine Cervical Neoplasms - radiotherapy ; Uterine Cervical Neoplasms - therapy ; Xenograft Model Antitumor Assays</subject><ispartof>Gene therapy, 2009-09, Vol.16 (9), p.1111-1121</ispartof><rights>Macmillan Publishers Limited 2009</rights><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2009</rights><rights>Macmillan Publishers Limited 2009.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-71def15b3c57bc74da15915f5389c7d3e02c9139eeed9414d55645ca1b80cea73</citedby><cites>FETCH-LOGICAL-c469t-71def15b3c57bc74da15915f5389c7d3e02c9139eeed9414d55645ca1b80cea73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gt.2009.72$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gt.2009.72$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21879375$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19494843$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, J</creatorcontrib><creatorcontrib>Kim, P-H</creatorcontrib><creatorcontrib>Yoo, J Y</creatorcontrib><creatorcontrib>Yoon, A-R</creatorcontrib><creatorcontrib>Choi, H J</creatorcontrib><creatorcontrib>Seong, J</creatorcontrib><creatorcontrib>Kim, I-W</creatorcontrib><creatorcontrib>Kim, J-H</creatorcontrib><creatorcontrib>Yun, C-O</creatorcontrib><title>Double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus in combination with radiotherapy elicits an enhanced anti-tumor effect</title><title>Gene therapy</title><addtitle>Gene Ther</addtitle><addtitle>Gene Ther</addtitle><description>Radiation therapy, a mainstay for anti-tumor therapeutic regimens for a variety of tumor types, triggers tumor cell apoptotic pathways by either directly eliciting DNA damage or indirectly inducing the formation of oxygen radicals. In an effort to augment radiation therapy, we generated a double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus (Ad−ΔE1B19/55). In combination with radiotherapy, greater cytotoxicity was observed for Ad−ΔE1B19/55 than for the single E1B 55 kDa-deleted oncolytic Ad (Ad−ΔE1B55). Consistent with this observation, higher levels of p53, phospho-p53, phospho-Chk1, phospho-Chk2, PI3K (phosphatidylinositol-3-kinase), phospho-AKT, cytochrome c, and cleavage of PARP (poly (ADP-ribose) polymerase) and caspase-3 were observed in cells treated with Ad−ΔE1B19/55 compared with those treated with Ad−ΔE1B55, indicating that the E1B 19 kDa present in Ad−ΔE1B55 may partially block radiation-induced apoptosis. A significant therapeutic benefit was also observed
in vivo
when oncolytic Ads and radiation were combined. Tumors treated with Ad−ΔE1B19/55 and radiation showed large areas of necrosis and apoptosis with the corresponding induction of p53. Finally, consistent with
in vitro
observations, the combination of Ad−ΔE1B19/55 and radiation was more efficacious than the combination of Ad−ΔE1B55 and radiation. Taken together, these results present a strong therapeutic rationale for combining radiation therapy with E1B 19 kDa-deleted oncolytic Ad.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adenoviridae - genetics</subject><subject>Adenovirus E1B Proteins - genetics</subject><subject>Adenoviruses</subject><subject>Ageing, cell death</subject><subject>AKT protein</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Applied cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>CHK1 protein</subject><subject>Combined Modality Therapy</subject><subject>Cytochrome c</subject><subject>Cytotoxicity</subject><subject>DNA damage</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>Gene Therapy</subject><subject>Genetic aspects</subject><subject>Genetic vectors</subject><subject>Health. Pharmaceutical industry</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Industrial applications and implications. Economical aspects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methods</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Molecular and cellular biology</subject><subject>Nanotechnology</subject><subject>Oncolysis</subject><subject>Oncolytic Virotherapy - methods</subject><subject>Oncolytic Viruses - genetics</subject><subject>original-article</subject><subject>p53 Protein</subject><subject>Patient outcomes</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Radiation therapy</subject><subject>Radiotherapy</subject><subject>Ribose</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Tumors</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Uterine Cervical Neoplasms - radiotherapy</subject><subject>Uterine Cervical Neoplasms - therapy</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0969-7128</issn><issn>1476-5462</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp10s1u1DAQAOAIgWgpXHgAZIEAAcpix3YcH0tboFIlJH7Okdee7Lok9mI7wN649jV5Ehx2xbKoyAdLk88zsWeK4j7BM4Jp83KRZhXGciaqG8UhYaIuOaurm8UhlrUsBamag-JOjJcYYyaa6nZxQCSTrGH0sLg69eO8B3RGXiEif_64-nyqSqSc-R3hfBsx0EMCg7zTvl8nq5Ey4PxXG8aIrEPaD3PrVLLeoW82LVFQxvq0hKBWawS91TbFnBaBWyqncyblki3TOPiAoOtAp7vFrU71Ee5t96Pi0-uzjydvy4t3b85Pji9KzWqZ8nUMdITPqeZirgUzinBJeMdpI7UwFHClJaESAIxkhBnOa8a1IvMGa1CCHhVPN3lXwX8ZIaZ2sFFD3ysHfoytoJQJ3Eia5aN_5KUfg8s_11Y1YzWtG0GyevhfRRrBOBZ4l2qhemit63wKSk-F2-Mqt4k2dTUVnF2j8jIwWO0ddDbH9w482zuQTYLvaaHGGNvzD-_37ZO_7BJUn5bR9-PUs7gPn2-gDj7GAF27CnZQYd0S3E4D1y5SOw1cK6qMH2xvP84HMDu6nbAMHm-Bilr1Xcjtt_GPm55IUsGze7FxMX9yCwi7Z7ym7C_5QOi9</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Kim, J</creator><creator>Kim, P-H</creator><creator>Yoo, J Y</creator><creator>Yoon, A-R</creator><creator>Choi, H J</creator><creator>Seong, J</creator><creator>Kim, I-W</creator><creator>Kim, J-H</creator><creator>Yun, C-O</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090901</creationdate><title>Double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus in combination with radiotherapy elicits an enhanced anti-tumor effect</title><author>Kim, J ; Kim, P-H ; Yoo, J Y ; Yoon, A-R ; Choi, H J ; Seong, J ; Kim, I-W ; Kim, J-H ; Yun, C-O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-71def15b3c57bc74da15915f5389c7d3e02c9139eeed9414d55645ca1b80cea73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Adenoviridae - genetics</topic><topic>Adenovirus E1B Proteins - genetics</topic><topic>Adenoviruses</topic><topic>Ageing, cell death</topic><topic>AKT protein</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Applied cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Care and treatment</topic><topic>Caspase-3</topic><topic>Cell Biology</topic><topic>Cell physiology</topic><topic>CHK1 protein</topic><topic>Combined Modality Therapy</topic><topic>Cytochrome c</topic><topic>Cytotoxicity</topic><topic>DNA damage</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>Gene Therapy</topic><topic>Genetic aspects</topic><topic>Genetic vectors</topic><topic>Health. Pharmaceutical industry</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Industrial applications and implications. Economical aspects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methods</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Molecular and cellular biology</topic><topic>Nanotechnology</topic><topic>Oncolysis</topic><topic>Oncolytic Virotherapy - methods</topic><topic>Oncolytic Viruses - genetics</topic><topic>original-article</topic><topic>p53 Protein</topic><topic>Patient outcomes</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Radiation therapy</topic><topic>Radiotherapy</topic><topic>Ribose</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Tumors</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Uterine Cervical Neoplasms - radiotherapy</topic><topic>Uterine Cervical Neoplasms - therapy</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, J</creatorcontrib><creatorcontrib>Kim, P-H</creatorcontrib><creatorcontrib>Yoo, J Y</creatorcontrib><creatorcontrib>Yoon, A-R</creatorcontrib><creatorcontrib>Choi, H J</creatorcontrib><creatorcontrib>Seong, J</creatorcontrib><creatorcontrib>Kim, I-W</creatorcontrib><creatorcontrib>Kim, J-H</creatorcontrib><creatorcontrib>Yun, C-O</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>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS 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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, J</au><au>Kim, P-H</au><au>Yoo, J Y</au><au>Yoon, A-R</au><au>Choi, H J</au><au>Seong, J</au><au>Kim, I-W</au><au>Kim, J-H</au><au>Yun, C-O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus in combination with radiotherapy elicits an enhanced anti-tumor effect</atitle><jtitle>Gene therapy</jtitle><stitle>Gene Ther</stitle><addtitle>Gene Ther</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>16</volume><issue>9</issue><spage>1111</spage><epage>1121</epage><pages>1111-1121</pages><issn>0969-7128</issn><eissn>1476-5462</eissn><abstract>Radiation therapy, a mainstay for anti-tumor therapeutic regimens for a variety of tumor types, triggers tumor cell apoptotic pathways by either directly eliciting DNA damage or indirectly inducing the formation of oxygen radicals. In an effort to augment radiation therapy, we generated a double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus (Ad−ΔE1B19/55). In combination with radiotherapy, greater cytotoxicity was observed for Ad−ΔE1B19/55 than for the single E1B 55 kDa-deleted oncolytic Ad (Ad−ΔE1B55). Consistent with this observation, higher levels of p53, phospho-p53, phospho-Chk1, phospho-Chk2, PI3K (phosphatidylinositol-3-kinase), phospho-AKT, cytochrome c, and cleavage of PARP (poly (ADP-ribose) polymerase) and caspase-3 were observed in cells treated with Ad−ΔE1B19/55 compared with those treated with Ad−ΔE1B55, indicating that the E1B 19 kDa present in Ad−ΔE1B55 may partially block radiation-induced apoptosis. A significant therapeutic benefit was also observed
in vivo
when oncolytic Ads and radiation were combined. Tumors treated with Ad−ΔE1B19/55 and radiation showed large areas of necrosis and apoptosis with the corresponding induction of p53. Finally, consistent with
in vitro
observations, the combination of Ad−ΔE1B19/55 and radiation was more efficacious than the combination of Ad−ΔE1B55 and radiation. Taken together, these results present a strong therapeutic rationale for combining radiation therapy with E1B 19 kDa-deleted oncolytic Ad.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19494843</pmid><doi>10.1038/gt.2009.72</doi><tpages>11</tpages></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Adenoviridae - genetics Adenovirus E1B Proteins - genetics Adenoviruses Ageing, cell death AKT protein Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Apoptosis Apoptosis - genetics Applied cell therapy and gene therapy Biological and medical sciences Biomedical and Life Sciences Biomedicine Biotechnology Cancer Care and treatment Caspase-3 Cell Biology Cell physiology CHK1 protein Combined Modality Therapy Cytochrome c Cytotoxicity DNA damage Female Fundamental and applied biological sciences. Psychology Gene Expression Gene Therapy Genetic aspects Genetic vectors Health. Pharmaceutical industry Human Genetics Humans Industrial applications and implications. Economical aspects Male Medical sciences Methods Mice Mice, Inbred BALB C Mice, Nude Molecular and cellular biology Nanotechnology Oncolysis Oncolytic Virotherapy - methods Oncolytic Viruses - genetics original-article p53 Protein Patient outcomes Poly(ADP-ribose) polymerase Radiation therapy Radiotherapy Ribose Transfusions. Complications. Transfusion reactions. Cell and gene therapy Tumors Uterine Cervical Neoplasms - pathology Uterine Cervical Neoplasms - radiotherapy Uterine Cervical Neoplasms - therapy Xenograft Model Antitumor Assays |
title | Double E1B 19 kDa- and E1B 55 kDa-deleted oncolytic adenovirus in combination with radiotherapy elicits an enhanced anti-tumor effect |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T04%3A19%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Double%20E1B%2019%E2%80%89kDa-%20and%20E1B%2055%E2%80%89kDa-deleted%20oncolytic%20adenovirus%20in%20combination%20with%20radiotherapy%20elicits%20an%20enhanced%20anti-tumor%20effect&rft.jtitle=Gene%20therapy&rft.au=Kim,%20J&rft.date=2009-09-01&rft.volume=16&rft.issue=9&rft.spage=1111&rft.epage=1121&rft.pages=1111-1121&rft.issn=0969-7128&rft.eissn=1476-5462&rft_id=info:doi/10.1038/gt.2009.72&rft_dat=%3Cgale_proqu%3EA209638623%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=218745070&rft_id=info:pmid/19494843&rft_galeid=A209638623&rfr_iscdi=true |