An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer
Due to recurrence and resistance to chemotherapy, the current standard therapeutics are not fully effective against ovarian cancer. Therefore, we aimed to find an effective approach to improve the prognosis and therapy of ovarian cancer. NG34ScFvPD-1 is a modified oncolytic herpes simplex virus NG34...
Gespeichert in:
| Veröffentlicht in: | Archives of virology 2023-04, Vol.168 (4), p.128-128, Article 128 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 128 |
|---|---|
| container_issue | 4 |
| container_start_page | 128 |
| container_title | Archives of virology |
| container_volume | 168 |
| creator | Huang, Shanying Hu, Haiyan Tang, Guoling Liu, Kai Luo, Zhihua Zeng, Weiwei |
| description | Due to recurrence and resistance to chemotherapy, the current standard therapeutics are not fully effective against ovarian cancer. Therefore, we aimed to find an effective approach to improve the prognosis and therapy of ovarian cancer. NG34ScFvPD-1 is a modified oncolytic herpes simplex virus NG34 strain that expresses a single-chain antibody against programmed cell death protein 1 (PD-1) (ScFvPD-1). We assessed its efficacy and its regulatory mechanism in a mouse model of ovarian cancer. Enzyme-linked immunosorbent assay and western blot techniques were used to measure protein expression. Oncolysis caused by NG34ScFvPD-1 was examined using cytotoxicity and replication assays. The mechanism by which NG34ScFvPD-1 regulates apoptosis of ovarian cancer cells
in vitro
was also evaluated. We assessed the antitumor immunity and therapeutic potency of NG34ScFvPD-1 in combination with a phosphoinositide 3-kinase (PI3K) inhibitor. We found that NG34ScFvPD-1-infected ovarian cancer cells expressed and secreted ScFvPD-1, which bound mouse PD-1. The insertion of the ScFvPD-1 sequence did not inhibit the oncolytic activity of NG34ScFvPD-1, which induced apoptosis of ovarian cancer cells via the caspase-dependent pathway
in vitro
and activated the PI3K/AKT signaling pathway. Synergy was observed between NG34ScFvPD-1 and a PI3K inhibitor, and the combination was able to suppress tumor development, to prolong survival, and to elicit potent antitumor immunity. Thus, inhibition of PI3K enhanced the potent antitumor immunity induced by NG34ScFvPD-1 against ovarian cancer. |
| doi_str_mv | 10.1007/s00705-023-05754-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2793984890</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2793984890</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-3a988046fdd9512e5554bacab23ef278d62939bc78d4cc9984ae6cd99f7cb3ec3</originalsourceid><addsrcrecordid>eNp9kc1u1DAUhS0EokPhBVigK7FhE3BsZ2Ivq5afikp0AevIcW4yrhI72E7V9AH7XHhmCkgs2PhaPt8519Ih5HVJ35eU1h9iPmhVUMYLWtWVKMonZFMKzgpZK_mUbCinopBbKk_IixhvKM0PvHpOTnhNKRNcbMjDmQPvjB_XZA3sMMwYIdppHvEObm1YIqR1RighpqCtA7ybA8Zo3QAa9mPEwuz2yq0OVrcjQsDBegfaJdv6boU-6GFCl0APmYsJri-KMstdTri-5F_Bup1tbfIB4uowDPYeIXnA0RqbDjlpmbJqp2lxNq3ZAP6wzoHRzmB4SZ71eoz46nGekh-fPn4__1Jcfft8eX52VRheV6ngWklJxbbvOlWVDKuqEq02umUce1bLbssUV63JN2GMUlJo3JpOqb42LUfDT8m7Y-4c_M8FY2omGw2Oo3bol9iwOvulkIpm9O0_6I1fgsu_O1Cs4oLtKXakTPAxBuybOdhJh7UpabNvuTm23OSWm0PLTZlNbx6jl3bC7o_ld60Z4EcgZskNGP7u_k_sL4Fwtnk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2793253420</pqid></control><display><type>article</type><title>An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Huang, Shanying ; Hu, Haiyan ; Tang, Guoling ; Liu, Kai ; Luo, Zhihua ; Zeng, Weiwei</creator><creatorcontrib>Huang, Shanying ; Hu, Haiyan ; Tang, Guoling ; Liu, Kai ; Luo, Zhihua ; Zeng, Weiwei</creatorcontrib><description>Due to recurrence and resistance to chemotherapy, the current standard therapeutics are not fully effective against ovarian cancer. Therefore, we aimed to find an effective approach to improve the prognosis and therapy of ovarian cancer. NG34ScFvPD-1 is a modified oncolytic herpes simplex virus NG34 strain that expresses a single-chain antibody against programmed cell death protein 1 (PD-1) (ScFvPD-1). We assessed its efficacy and its regulatory mechanism in a mouse model of ovarian cancer. Enzyme-linked immunosorbent assay and western blot techniques were used to measure protein expression. Oncolysis caused by NG34ScFvPD-1 was examined using cytotoxicity and replication assays. The mechanism by which NG34ScFvPD-1 regulates apoptosis of ovarian cancer cells
in vitro
was also evaluated. We assessed the antitumor immunity and therapeutic potency of NG34ScFvPD-1 in combination with a phosphoinositide 3-kinase (PI3K) inhibitor. We found that NG34ScFvPD-1-infected ovarian cancer cells expressed and secreted ScFvPD-1, which bound mouse PD-1. The insertion of the ScFvPD-1 sequence did not inhibit the oncolytic activity of NG34ScFvPD-1, which induced apoptosis of ovarian cancer cells via the caspase-dependent pathway
in vitro
and activated the PI3K/AKT signaling pathway. Synergy was observed between NG34ScFvPD-1 and a PI3K inhibitor, and the combination was able to suppress tumor development, to prolong survival, and to elicit potent antitumor immunity. Thus, inhibition of PI3K enhanced the potent antitumor immunity induced by NG34ScFvPD-1 against ovarian cancer.</description><identifier>ISSN: 0304-8608</identifier><identifier>EISSN: 1432-8798</identifier><identifier>DOI: 10.1007/s00705-023-05754-1</identifier><identifier>PMID: 37002434</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Caspase ; Cell death ; Cell Line, Tumor ; Chemotherapy ; Cytotoxicity ; Enzyme-linked immunosorbent assay ; Female ; Herpes simplex ; Herpes viruses ; Herpesvirus 1, Human ; Humans ; Immunity ; Infectious Diseases ; Kinases ; Medical Microbiology ; Medical prognosis ; Mice ; Oncolysis ; Oncolytic Virotherapy - methods ; Oncolytic Viruses - genetics ; Original Article ; Ovarian cancer ; Ovarian Neoplasms - pathology ; Ovarian Neoplasms - therapy ; PD-1 protein ; Phosphatidylinositol 3-Kinases ; Phosphoinositide-3 Kinase Inhibitors ; Programmed Cell Death 1 Receptor ; Signal transduction ; Single-Chain Antibodies - genetics ; Synergism ; Variable region ; Virology</subject><ispartof>Archives of virology, 2023-04, Vol.168 (4), p.128-128, Article 128</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-3a988046fdd9512e5554bacab23ef278d62939bc78d4cc9984ae6cd99f7cb3ec3</citedby><cites>FETCH-LOGICAL-c375t-3a988046fdd9512e5554bacab23ef278d62939bc78d4cc9984ae6cd99f7cb3ec3</cites><orcidid>0000-0003-3158-6959</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00705-023-05754-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00705-023-05754-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37002434$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Shanying</creatorcontrib><creatorcontrib>Hu, Haiyan</creatorcontrib><creatorcontrib>Tang, Guoling</creatorcontrib><creatorcontrib>Liu, Kai</creatorcontrib><creatorcontrib>Luo, Zhihua</creatorcontrib><creatorcontrib>Zeng, Weiwei</creatorcontrib><title>An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer</title><title>Archives of virology</title><addtitle>Arch Virol</addtitle><addtitle>Arch Virol</addtitle><description>Due to recurrence and resistance to chemotherapy, the current standard therapeutics are not fully effective against ovarian cancer. Therefore, we aimed to find an effective approach to improve the prognosis and therapy of ovarian cancer. NG34ScFvPD-1 is a modified oncolytic herpes simplex virus NG34 strain that expresses a single-chain antibody against programmed cell death protein 1 (PD-1) (ScFvPD-1). We assessed its efficacy and its regulatory mechanism in a mouse model of ovarian cancer. Enzyme-linked immunosorbent assay and western blot techniques were used to measure protein expression. Oncolysis caused by NG34ScFvPD-1 was examined using cytotoxicity and replication assays. The mechanism by which NG34ScFvPD-1 regulates apoptosis of ovarian cancer cells
in vitro
was also evaluated. We assessed the antitumor immunity and therapeutic potency of NG34ScFvPD-1 in combination with a phosphoinositide 3-kinase (PI3K) inhibitor. We found that NG34ScFvPD-1-infected ovarian cancer cells expressed and secreted ScFvPD-1, which bound mouse PD-1. The insertion of the ScFvPD-1 sequence did not inhibit the oncolytic activity of NG34ScFvPD-1, which induced apoptosis of ovarian cancer cells via the caspase-dependent pathway
in vitro
and activated the PI3K/AKT signaling pathway. Synergy was observed between NG34ScFvPD-1 and a PI3K inhibitor, and the combination was able to suppress tumor development, to prolong survival, and to elicit potent antitumor immunity. Thus, inhibition of PI3K enhanced the potent antitumor immunity induced by NG34ScFvPD-1 against ovarian cancer.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Herpes simplex</subject><subject>Herpes viruses</subject><subject>Herpesvirus 1, Human</subject><subject>Humans</subject><subject>Immunity</subject><subject>Infectious Diseases</subject><subject>Kinases</subject><subject>Medical Microbiology</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Oncolysis</subject><subject>Oncolytic Virotherapy - methods</subject><subject>Oncolytic Viruses - genetics</subject><subject>Original Article</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Ovarian Neoplasms - therapy</subject><subject>PD-1 protein</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>Phosphoinositide-3 Kinase Inhibitors</subject><subject>Programmed Cell Death 1 Receptor</subject><subject>Signal transduction</subject><subject>Single-Chain Antibodies - genetics</subject><subject>Synergism</subject><subject>Variable region</subject><subject>Virology</subject><issn>0304-8608</issn><issn>1432-8798</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1DAUhS0EokPhBVigK7FhE3BsZ2Ivq5afikp0AevIcW4yrhI72E7V9AH7XHhmCkgs2PhaPt8519Ih5HVJ35eU1h9iPmhVUMYLWtWVKMonZFMKzgpZK_mUbCinopBbKk_IixhvKM0PvHpOTnhNKRNcbMjDmQPvjB_XZA3sMMwYIdppHvEObm1YIqR1RighpqCtA7ybA8Zo3QAa9mPEwuz2yq0OVrcjQsDBegfaJdv6boU-6GFCl0APmYsJri-KMstdTri-5F_Bup1tbfIB4uowDPYeIXnA0RqbDjlpmbJqp2lxNq3ZAP6wzoHRzmB4SZ71eoz46nGekh-fPn4__1Jcfft8eX52VRheV6ngWklJxbbvOlWVDKuqEq02umUce1bLbssUV63JN2GMUlJo3JpOqb42LUfDT8m7Y-4c_M8FY2omGw2Oo3bol9iwOvulkIpm9O0_6I1fgsu_O1Cs4oLtKXakTPAxBuybOdhJh7UpabNvuTm23OSWm0PLTZlNbx6jl3bC7o_ld60Z4EcgZskNGP7u_k_sL4Fwtnk</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Huang, Shanying</creator><creator>Hu, Haiyan</creator><creator>Tang, Guoling</creator><creator>Liu, Kai</creator><creator>Luo, Zhihua</creator><creator>Zeng, Weiwei</creator><general>Springer Vienna</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</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>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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3158-6959</orcidid></search><sort><creationdate>20230401</creationdate><title>An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer</title><author>Huang, Shanying ; Hu, Haiyan ; Tang, Guoling ; Liu, Kai ; Luo, Zhihua ; Zeng, Weiwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-3a988046fdd9512e5554bacab23ef278d62939bc78d4cc9984ae6cd99f7cb3ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspase</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Herpes simplex</topic><topic>Herpes viruses</topic><topic>Herpesvirus 1, Human</topic><topic>Humans</topic><topic>Immunity</topic><topic>Infectious Diseases</topic><topic>Kinases</topic><topic>Medical Microbiology</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>Oncolysis</topic><topic>Oncolytic Virotherapy - methods</topic><topic>Oncolytic Viruses - genetics</topic><topic>Original Article</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Ovarian Neoplasms - therapy</topic><topic>PD-1 protein</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>Phosphoinositide-3 Kinase Inhibitors</topic><topic>Programmed Cell Death 1 Receptor</topic><topic>Signal transduction</topic><topic>Single-Chain Antibodies - genetics</topic><topic>Synergism</topic><topic>Variable region</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Shanying</creatorcontrib><creatorcontrib>Hu, Haiyan</creatorcontrib><creatorcontrib>Tang, Guoling</creatorcontrib><creatorcontrib>Liu, Kai</creatorcontrib><creatorcontrib>Luo, Zhihua</creatorcontrib><creatorcontrib>Zeng, Weiwei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>Biology Database (Alumni Edition)</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>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>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>Biological Science Database</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Shanying</au><au>Hu, Haiyan</au><au>Tang, Guoling</au><au>Liu, Kai</au><au>Luo, Zhihua</au><au>Zeng, Weiwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer</atitle><jtitle>Archives of virology</jtitle><stitle>Arch Virol</stitle><addtitle>Arch Virol</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>168</volume><issue>4</issue><spage>128</spage><epage>128</epage><pages>128-128</pages><artnum>128</artnum><issn>0304-8608</issn><eissn>1432-8798</eissn><abstract>Due to recurrence and resistance to chemotherapy, the current standard therapeutics are not fully effective against ovarian cancer. Therefore, we aimed to find an effective approach to improve the prognosis and therapy of ovarian cancer. NG34ScFvPD-1 is a modified oncolytic herpes simplex virus NG34 strain that expresses a single-chain antibody against programmed cell death protein 1 (PD-1) (ScFvPD-1). We assessed its efficacy and its regulatory mechanism in a mouse model of ovarian cancer. Enzyme-linked immunosorbent assay and western blot techniques were used to measure protein expression. Oncolysis caused by NG34ScFvPD-1 was examined using cytotoxicity and replication assays. The mechanism by which NG34ScFvPD-1 regulates apoptosis of ovarian cancer cells
in vitro
was also evaluated. We assessed the antitumor immunity and therapeutic potency of NG34ScFvPD-1 in combination with a phosphoinositide 3-kinase (PI3K) inhibitor. We found that NG34ScFvPD-1-infected ovarian cancer cells expressed and secreted ScFvPD-1, which bound mouse PD-1. The insertion of the ScFvPD-1 sequence did not inhibit the oncolytic activity of NG34ScFvPD-1, which induced apoptosis of ovarian cancer cells via the caspase-dependent pathway
in vitro
and activated the PI3K/AKT signaling pathway. Synergy was observed between NG34ScFvPD-1 and a PI3K inhibitor, and the combination was able to suppress tumor development, to prolong survival, and to elicit potent antitumor immunity. Thus, inhibition of PI3K enhanced the potent antitumor immunity induced by NG34ScFvPD-1 against ovarian cancer.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>37002434</pmid><doi>10.1007/s00705-023-05754-1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-3158-6959</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-8608 |
| ispartof | Archives of virology, 2023-04, Vol.168 (4), p.128-128, Article 128 |
| issn | 0304-8608 1432-8798 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2793984890 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals Apoptosis Biomedical and Life Sciences Biomedicine Caspase Cell death Cell Line, Tumor Chemotherapy Cytotoxicity Enzyme-linked immunosorbent assay Female Herpes simplex Herpes viruses Herpesvirus 1, Human Humans Immunity Infectious Diseases Kinases Medical Microbiology Medical prognosis Mice Oncolysis Oncolytic Virotherapy - methods Oncolytic Viruses - genetics Original Article Ovarian cancer Ovarian Neoplasms - pathology Ovarian Neoplasms - therapy PD-1 protein Phosphatidylinositol 3-Kinases Phosphoinositide-3 Kinase Inhibitors Programmed Cell Death 1 Receptor Signal transduction Single-Chain Antibodies - genetics Synergism Variable region Virology |
| title | An oncolytic herpes simplex virus type 1 strain expressing a single-chain variable region antibody fragment against PD-1 and a PI3K inhibitor synergize to elicit antitumor immunity in ovarian cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T13%3A48%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=An%20oncolytic%20herpes%20simplex%20virus%20type%201%20strain%20expressing%20a%20single-chain%20variable%20region%20antibody%20fragment%20against%20PD-1%20and%20a%20PI3K%20inhibitor%20synergize%20to%20elicit%20antitumor%20immunity%20in%20ovarian%20cancer&rft.jtitle=Archives%20of%20virology&rft.au=Huang,%20Shanying&rft.date=2023-04-01&rft.volume=168&rft.issue=4&rft.spage=128&rft.epage=128&rft.pages=128-128&rft.artnum=128&rft.issn=0304-8608&rft.eissn=1432-8798&rft_id=info:doi/10.1007/s00705-023-05754-1&rft_dat=%3Cproquest_cross%3E2793984890%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2793253420&rft_id=info:pmid/37002434&rfr_iscdi=true |