Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors
CD30 is a member of the tumor necrosis factor receptor family. Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggress...
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Veröffentlicht in: | Blood 2006-07, Vol.108 (2), p.705-710 |
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creator | Zhang, Meili Yao, Zhengsheng Zhang, Zhuo Garmestani, Kayhan Goldman, Carolyn K. Ravetch, Jeffrey V. Janik, John Brechbiel, Martin W. Waldmann, Thomas A. |
description | CD30 is a member of the tumor necrosis factor receptor family. Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non-Hodgkin lymphomas characterized by the strong expression of CD30. We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL. The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common γ chain–deficient (FcRγ–/–) mice. HeFi-1, given at a dose of 100 μg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRγ–/– mice (P < .01) as compared with the control groups. In vitro studies showed that HeFi-1 inhibited the proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation. We demonstrated that the expression of FcRγ on polymorphonuclear leukocytes and monocytes was not required for HeFi-1–mediated tumor growth inhibition in vivo, although it was required for daclizumab. |
doi_str_mv | 10.1182/blood-2005-11-4607 |
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Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non-Hodgkin lymphomas characterized by the strong expression of CD30. We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL. The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common γ chain–deficient (FcRγ–/–) mice. HeFi-1, given at a dose of 100 μg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRγ–/– mice (P < .01) as compared with the control groups. In vitro studies showed that HeFi-1 inhibited the proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation. We demonstrated that the expression of FcRγ on polymorphonuclear leukocytes and monocytes was not required for HeFi-1–mediated tumor growth inhibition in vivo, although it was required for daclizumab.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2005-11-4607</identifier><identifier>PMID: 16551968</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Animals ; Antibodies, Monoclonal - pharmacology ; Antibodies, Monoclonal - therapeutic use ; Antibodies, Monoclonal, Humanized ; Antigens, Neoplasm - immunology ; Antineoplastic agents ; Biological and medical sciences ; Cell Proliferation - drug effects ; Daclizumab ; Disease Models, Animal ; Hematologic and hematopoietic diseases ; Humans ; Immunoglobulin G - pharmacology ; Immunotherapy ; Immunotherapy - methods ; Ki-1 Antigen - immunology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoma, Large-Cell, Anaplastic - drug therapy ; Medical sciences ; Mice ; Mice, Knockout ; Mice, SCID ; Neoplasia ; Neoplasm Transplantation ; Pharmacology. Drug treatments ; Receptors, Fc - metabolism ; Transplantation, Heterologous ; Tumor Burden - drug effects</subject><ispartof>Blood, 2006-07, Vol.108 (2), p.705-710</ispartof><rights>2006 American Society of Hematology</rights><rights>2006 INIST-CNRS</rights><rights>Copyright © 2006, The American Society of Hematology 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-d82b0d877cf0814ce32063e0576c60f4cae1cc42f4b39279beacabd38b92dd03</citedby><cites>FETCH-LOGICAL-c483t-d82b0d877cf0814ce32063e0576c60f4cae1cc42f4b39279beacabd38b92dd03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17957196$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16551968$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Meili</creatorcontrib><creatorcontrib>Yao, Zhengsheng</creatorcontrib><creatorcontrib>Zhang, Zhuo</creatorcontrib><creatorcontrib>Garmestani, Kayhan</creatorcontrib><creatorcontrib>Goldman, Carolyn K.</creatorcontrib><creatorcontrib>Ravetch, Jeffrey V.</creatorcontrib><creatorcontrib>Janik, John</creatorcontrib><creatorcontrib>Brechbiel, Martin W.</creatorcontrib><creatorcontrib>Waldmann, Thomas A.</creatorcontrib><title>Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors</title><title>Blood</title><addtitle>Blood</addtitle><description>CD30 is a member of the tumor necrosis factor receptor family. Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non-Hodgkin lymphomas characterized by the strong expression of CD30. We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL. The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common γ chain–deficient (FcRγ–/–) mice. HeFi-1, given at a dose of 100 μg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRγ–/– mice (P < .01) as compared with the control groups. In vitro studies showed that HeFi-1 inhibited the proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation. We demonstrated that the expression of FcRγ on polymorphonuclear leukocytes and monocytes was not required for HeFi-1–mediated tumor growth inhibition in vivo, although it was required for daclizumab.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antibodies, Monoclonal, Humanized</subject><subject>Antigens, Neoplasm - immunology</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation - drug effects</subject><subject>Daclizumab</subject><subject>Disease Models, Animal</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunoglobulin G - pharmacology</subject><subject>Immunotherapy</subject><subject>Immunotherapy - methods</subject><subject>Ki-1 Antigen - immunology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoma, Large-Cell, Anaplastic - drug therapy</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, SCID</subject><subject>Neoplasia</subject><subject>Neoplasm Transplantation</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, Fc - metabolism</subject><subject>Transplantation, Heterologous</subject><subject>Tumor Burden - drug effects</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2OFCEUhStG47SjL-DCsNHVoED9UYkxMe20YzKJm9kTCm51YSioAapNP5DvKTXdcXTjinD5zuHknqJ4Tcl7Sjn70FvvNWaE1JhSXDWkfVJsaM04JoSRp8WGENLgqmvpRfEixh-E0Kpk9fPigjZ1TbuGb4pf18MAKpkDoDRCkPMRDT4giaYlGAdo8hos8gMal0k6JJ2crYzJKGRl2ANWYC2yx2ke_STRT5PG1SdzyeDtl5JkA-eV9U7ah2Hv9fEK3cDOYHqFtIeInE8owP1iQtatUWQybo92Kk8VzMmH-LJ4Nkgb4dX5vCzudtd32xt8-_3rt-3nW6wqXiasOeuJ5m2rBsJppaBkpCmB1G2jGjJUSgJVqmJD1Zcda7sepJK9LnnfMa1JeVl8OtnOSz-BVuBSkFbMwUwyHIWXRvz74swo9v4gKO_qinfZ4N3ZIPj7BWISk4nriqQDv0TR8IZ0Na8yyE6gCj7GAMOfTygRa7nioVyxlpvvYi03i978He9Rcm4zA2_PgIxK2iFIp0x85NqubjOYuY8nDvIuDwaCiMqAU6BzByoJ7c3_cvwGdwLGqw</recordid><startdate>20060715</startdate><enddate>20060715</enddate><creator>Zhang, Meili</creator><creator>Yao, Zhengsheng</creator><creator>Zhang, Zhuo</creator><creator>Garmestani, Kayhan</creator><creator>Goldman, Carolyn K.</creator><creator>Ravetch, Jeffrey V.</creator><creator>Janik, John</creator><creator>Brechbiel, Martin W.</creator><creator>Waldmann, Thomas A.</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><general>The American Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060715</creationdate><title>Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors</title><author>Zhang, Meili ; Yao, Zhengsheng ; Zhang, Zhuo ; Garmestani, Kayhan ; Goldman, Carolyn K. ; Ravetch, Jeffrey V. ; Janik, John ; Brechbiel, Martin W. ; Waldmann, Thomas A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-d82b0d877cf0814ce32063e0576c60f4cae1cc42f4b39279beacabd38b92dd03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antibodies, Monoclonal, Humanized</topic><topic>Antigens, Neoplasm - immunology</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation - drug effects</topic><topic>Daclizumab</topic><topic>Disease Models, Animal</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunoglobulin G - pharmacology</topic><topic>Immunotherapy</topic><topic>Immunotherapy - methods</topic><topic>Ki-1 Antigen - immunology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphoma, Large-Cell, Anaplastic - drug therapy</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, SCID</topic><topic>Neoplasia</topic><topic>Neoplasm Transplantation</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, Fc - metabolism</topic><topic>Transplantation, Heterologous</topic><topic>Tumor Burden - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Meili</creatorcontrib><creatorcontrib>Yao, Zhengsheng</creatorcontrib><creatorcontrib>Zhang, Zhuo</creatorcontrib><creatorcontrib>Garmestani, Kayhan</creatorcontrib><creatorcontrib>Goldman, Carolyn K.</creatorcontrib><creatorcontrib>Ravetch, Jeffrey V.</creatorcontrib><creatorcontrib>Janik, John</creatorcontrib><creatorcontrib>Brechbiel, Martin W.</creatorcontrib><creatorcontrib>Waldmann, Thomas A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Meili</au><au>Yao, Zhengsheng</au><au>Zhang, Zhuo</au><au>Garmestani, Kayhan</au><au>Goldman, Carolyn K.</au><au>Ravetch, Jeffrey V.</au><au>Janik, John</au><au>Brechbiel, Martin W.</au><au>Waldmann, Thomas A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2006-07-15</date><risdate>2006</risdate><volume>108</volume><issue>2</issue><spage>705</spage><epage>710</epage><pages>705-710</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>CD30 is a member of the tumor necrosis factor receptor family. Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non-Hodgkin lymphomas characterized by the strong expression of CD30. We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL. The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common γ chain–deficient (FcRγ–/–) mice. HeFi-1, given at a dose of 100 μg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRγ–/– mice (P < .01) as compared with the control groups. In vitro studies showed that HeFi-1 inhibited the proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation. We demonstrated that the expression of FcRγ on polymorphonuclear leukocytes and monocytes was not required for HeFi-1–mediated tumor growth inhibition in vivo, although it was required for daclizumab.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>16551968</pmid><doi>10.1182/blood-2005-11-4607</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Antigens, Neoplasm - immunology Antineoplastic agents Biological and medical sciences Cell Proliferation - drug effects Daclizumab Disease Models, Animal Hematologic and hematopoietic diseases Humans Immunoglobulin G - pharmacology Immunotherapy Immunotherapy - methods Ki-1 Antigen - immunology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoma, Large-Cell, Anaplastic - drug therapy Medical sciences Mice Mice, Knockout Mice, SCID Neoplasia Neoplasm Transplantation Pharmacology. Drug treatments Receptors, Fc - metabolism Transplantation, Heterologous Tumor Burden - drug effects |
title | Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors |
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