Nitric Oxide Accelerates Interleukin-13 Cytotoxin-Mediated Regression in Head and Neck Cancer Animal Model
Receptors for interleukin-13 (IL-13R) are overexpressed on several types of solid cancers including gliobastoma, renal cell carcinoma, AIDS Kaposi’s sarcoma, and head and neck cancer. Recombinant fusion proteins IL-13 cytotoxin (IL13-PE38QQR or IL13-PE38) have been developed to directly target IL-13...
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| Veröffentlicht in: | Clinical cancer research 2004-08, Vol.10 (15), p.5264-5270 |
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| creator | KAWAKAMI, Koji KAWAKAMI, Mariko PURI, Raj K |
| description | Receptors for interleukin-13 (IL-13R) are overexpressed on several types of solid cancers including gliobastoma, renal cell
carcinoma, AIDS Kaposi’s sarcoma, and head and neck cancer. Recombinant fusion proteins IL-13 cytotoxin (IL13-PE38QQR or IL13-PE38)
have been developed to directly target IL-13R-expressing cancer cells. Although it has been found that IL-13 cytotoxin has
a direct potent antitumor activity in vivo in nude mice models of human cancers, the involvement of indirect antitumor effecter molecules such as nitric oxide (NO)
is unknown. To address this issue, we assessed the effect of NO inhibiter N ω -monomethyl- l -arginine on IL-13 cytotoxin-mediated cytotoxicity and NO2/NO3 production in HN12 head and neck cancer cells. In addition,
antitumor effects and NO levels in HN12 and KCCT873 head and neck tumors xenografted s.c. in nude mice when treated with IL-13
cytotoxin were evaluated by tumor measurement, Western blot, and immunohistochemistry analyses. Pretreatment of animals with
N ω -monomethyl- l -arginine significantly decreased the NO levels and IL-13 cytotoxin-mediated antitumor effects. In addition, depletion of
macrophages, known to produce NO, also decreased antitumor activity of IL-13 cytotoxin. Based on these studies, we concluded
that NO accelerates antitumor effect of IL-13 cytotoxin on head and neck tumor cells. Because IL-13 cytotoxin is currently
being tested in the clinic for the treatment of patients with recurrent glioblastoma maltiforme, our current findings suggest
maintaining macrophage and NO-producing cellular function for optimal therapeutic effect of this targeted agent. |
| doi_str_mv | 10.1158/1078-0432.CCR-04-0314 |
| format | Article |
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carcinoma, AIDS Kaposi’s sarcoma, and head and neck cancer. Recombinant fusion proteins IL-13 cytotoxin (IL13-PE38QQR or IL13-PE38)
have been developed to directly target IL-13R-expressing cancer cells. Although it has been found that IL-13 cytotoxin has
a direct potent antitumor activity in vivo in nude mice models of human cancers, the involvement of indirect antitumor effecter molecules such as nitric oxide (NO)
is unknown. To address this issue, we assessed the effect of NO inhibiter N ω -monomethyl- l -arginine on IL-13 cytotoxin-mediated cytotoxicity and NO2/NO3 production in HN12 head and neck cancer cells. In addition,
antitumor effects and NO levels in HN12 and KCCT873 head and neck tumors xenografted s.c. in nude mice when treated with IL-13
cytotoxin were evaluated by tumor measurement, Western blot, and immunohistochemistry analyses. Pretreatment of animals with
N ω -monomethyl- l -arginine significantly decreased the NO levels and IL-13 cytotoxin-mediated antitumor effects. In addition, depletion of
macrophages, known to produce NO, also decreased antitumor activity of IL-13 cytotoxin. Based on these studies, we concluded
that NO accelerates antitumor effect of IL-13 cytotoxin on head and neck tumor cells. Because IL-13 cytotoxin is currently
being tested in the clinic for the treatment of patients with recurrent glioblastoma maltiforme, our current findings suggest
maintaining macrophage and NO-producing cellular function for optimal therapeutic effect of this targeted agent.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-04-0314</identifier><identifier>PMID: 15297430</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Western ; Cell Line, Tumor ; Cytotoxins - metabolism ; Disease Models, Animal ; Drug Synergism ; Enzyme Inhibitors - pharmacology ; Exotoxins ; Head and Neck Neoplasms - drug therapy ; Head and Neck Neoplasms - pathology ; Humans ; Immunohistochemistry ; Immunotoxins - pharmacology ; Interleukin-13 - biosynthesis ; Interleukin-13 - metabolism ; Interleukin-13 - pharmacology ; Macrophages - metabolism ; Medical sciences ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms - metabolism ; Nitric Oxide - metabolism ; omega-N-Methylarginine - pharmacology ; Pharmacology. Drug treatments ; Recombinant Fusion Proteins - chemistry ; Tumors</subject><ispartof>Clinical cancer research, 2004-08, Vol.10 (15), p.5264-5270</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-d7837b5fc58a32cc7f7373055fe5425b1f40581818698e1741fdfd338cb3b0083</citedby><cites>FETCH-LOGICAL-c447t-d7837b5fc58a32cc7f7373055fe5425b1f40581818698e1741fdfd338cb3b0083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16014644$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15297430$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KAWAKAMI, Koji</creatorcontrib><creatorcontrib>KAWAKAMI, Mariko</creatorcontrib><creatorcontrib>PURI, Raj K</creatorcontrib><title>Nitric Oxide Accelerates Interleukin-13 Cytotoxin-Mediated Regression in Head and Neck Cancer Animal Model</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Receptors for interleukin-13 (IL-13R) are overexpressed on several types of solid cancers including gliobastoma, renal cell
carcinoma, AIDS Kaposi’s sarcoma, and head and neck cancer. Recombinant fusion proteins IL-13 cytotoxin (IL13-PE38QQR or IL13-PE38)
have been developed to directly target IL-13R-expressing cancer cells. Although it has been found that IL-13 cytotoxin has
a direct potent antitumor activity in vivo in nude mice models of human cancers, the involvement of indirect antitumor effecter molecules such as nitric oxide (NO)
is unknown. To address this issue, we assessed the effect of NO inhibiter N ω -monomethyl- l -arginine on IL-13 cytotoxin-mediated cytotoxicity and NO2/NO3 production in HN12 head and neck cancer cells. In addition,
antitumor effects and NO levels in HN12 and KCCT873 head and neck tumors xenografted s.c. in nude mice when treated with IL-13
cytotoxin were evaluated by tumor measurement, Western blot, and immunohistochemistry analyses. Pretreatment of animals with
N ω -monomethyl- l -arginine significantly decreased the NO levels and IL-13 cytotoxin-mediated antitumor effects. In addition, depletion of
macrophages, known to produce NO, also decreased antitumor activity of IL-13 cytotoxin. Based on these studies, we concluded
that NO accelerates antitumor effect of IL-13 cytotoxin on head and neck tumor cells. Because IL-13 cytotoxin is currently
being tested in the clinic for the treatment of patients with recurrent glioblastoma maltiforme, our current findings suggest
maintaining macrophage and NO-producing cellular function for optimal therapeutic effect of this targeted agent.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Cytotoxins - metabolism</subject><subject>Disease Models, Animal</subject><subject>Drug Synergism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Exotoxins</subject><subject>Head and Neck Neoplasms - drug therapy</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Immunotoxins - pharmacology</subject><subject>Interleukin-13 - biosynthesis</subject><subject>Interleukin-13 - metabolism</subject><subject>Interleukin-13 - pharmacology</subject><subject>Macrophages - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasm Transplantation</subject><subject>Neoplasms - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>omega-N-Methylarginine - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Recombinant Fusion Proteins - chemistry</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkV1PHCEUhomxqVb7EzTc2KQXY2HgDOzlZtJWEz8SU68JAwcXnZ1RmE3135dxtzFc8JI853B4IOSEs3POQf_gTOmKSVGft-1dCRUTXO6RQw6gKlE3sF_yf-aAfMn5kTEuOZOfyQGHeqGkYIfk8SZOKTp6-xo90qVz2GOyE2Z6OUyYetw8xaHigrZv0ziNr-VwjT4WwtM7fEiYcxwHGgd6gdZTO3h6g-6JtnZwmOhyiGvb0-vRY39MPgXbZ_y624_I_a-ff9qL6ur292W7vKqclGqqvNJCdRAcaCtq51RQQgkGEBBkDR0PkoHmZTULjVxJHnzwQmjXiY4xLY7It23f5zS-bDBPZh1zeVdvBxw32fDFQmgJUEDYgi6NOScM5jmVcdOb4czMks0s0MwCTZFcgpkll7rT3QWbbo3-o2pntQBnO8BmZ_uQioyYP7imfEQj50bft9wqPqz-xoTGvWsrVtEmt3qfAwzUjRT_ALBIkeQ</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>KAWAKAMI, Koji</creator><creator>KAWAKAMI, Mariko</creator><creator>PURI, Raj K</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>7T5</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20040801</creationdate><title>Nitric Oxide Accelerates Interleukin-13 Cytotoxin-Mediated Regression in Head and Neck Cancer Animal Model</title><author>KAWAKAMI, Koji ; KAWAKAMI, Mariko ; PURI, Raj K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-d7837b5fc58a32cc7f7373055fe5425b1f40581818698e1741fdfd338cb3b0083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Cytotoxins - metabolism</topic><topic>Disease Models, Animal</topic><topic>Drug Synergism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Exotoxins</topic><topic>Head and Neck Neoplasms - drug therapy</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Immunotoxins - pharmacology</topic><topic>Interleukin-13 - biosynthesis</topic><topic>Interleukin-13 - metabolism</topic><topic>Interleukin-13 - pharmacology</topic><topic>Macrophages - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplasm Transplantation</topic><topic>Neoplasms - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>omega-N-Methylarginine - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Recombinant Fusion Proteins - chemistry</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KAWAKAMI, Koji</creatorcontrib><creatorcontrib>KAWAKAMI, Mariko</creatorcontrib><creatorcontrib>PURI, Raj K</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>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KAWAKAMI, Koji</au><au>KAWAKAMI, Mariko</au><au>PURI, Raj K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric Oxide Accelerates Interleukin-13 Cytotoxin-Mediated Regression in Head and Neck Cancer Animal Model</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>10</volume><issue>15</issue><spage>5264</spage><epage>5270</epage><pages>5264-5270</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Receptors for interleukin-13 (IL-13R) are overexpressed on several types of solid cancers including gliobastoma, renal cell
carcinoma, AIDS Kaposi’s sarcoma, and head and neck cancer. Recombinant fusion proteins IL-13 cytotoxin (IL13-PE38QQR or IL13-PE38)
have been developed to directly target IL-13R-expressing cancer cells. Although it has been found that IL-13 cytotoxin has
a direct potent antitumor activity in vivo in nude mice models of human cancers, the involvement of indirect antitumor effecter molecules such as nitric oxide (NO)
is unknown. To address this issue, we assessed the effect of NO inhibiter N ω -monomethyl- l -arginine on IL-13 cytotoxin-mediated cytotoxicity and NO2/NO3 production in HN12 head and neck cancer cells. In addition,
antitumor effects and NO levels in HN12 and KCCT873 head and neck tumors xenografted s.c. in nude mice when treated with IL-13
cytotoxin were evaluated by tumor measurement, Western blot, and immunohistochemistry analyses. Pretreatment of animals with
N ω -monomethyl- l -arginine significantly decreased the NO levels and IL-13 cytotoxin-mediated antitumor effects. In addition, depletion of
macrophages, known to produce NO, also decreased antitumor activity of IL-13 cytotoxin. Based on these studies, we concluded
that NO accelerates antitumor effect of IL-13 cytotoxin on head and neck tumor cells. Because IL-13 cytotoxin is currently
being tested in the clinic for the treatment of patients with recurrent glioblastoma maltiforme, our current findings suggest
maintaining macrophage and NO-producing cellular function for optimal therapeutic effect of this targeted agent.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15297430</pmid><doi>10.1158/1078-0432.CCR-04-0314</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2004-08, Vol.10 (15), p.5264-5270 |
| issn | 1078-0432 1557-3265 |
| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic agents Biological and medical sciences Blotting, Western Cell Line, Tumor Cytotoxins - metabolism Disease Models, Animal Drug Synergism Enzyme Inhibitors - pharmacology Exotoxins Head and Neck Neoplasms - drug therapy Head and Neck Neoplasms - pathology Humans Immunohistochemistry Immunotoxins - pharmacology Interleukin-13 - biosynthesis Interleukin-13 - metabolism Interleukin-13 - pharmacology Macrophages - metabolism Medical sciences Mice Mice, Nude Neoplasm Transplantation Neoplasms - metabolism Nitric Oxide - metabolism omega-N-Methylarginine - pharmacology Pharmacology. Drug treatments Recombinant Fusion Proteins - chemistry Tumors |
| title | Nitric Oxide Accelerates Interleukin-13 Cytotoxin-Mediated Regression in Head and Neck Cancer Animal Model |
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