Antibody-Dependent Cellular Cytotoxicity Mediated by Cetuximab against Lung Cancer Cell Lines
Purpose: Epidermal growth factor receptor (EGFR) is commonly overexpressed in lung cancer. Cetuximab is a chimeric mouse-human antibody targeted against EGFR. Compared with its inhibitory properties, its immunologic mechanisms have not been well studied. In this study, we investigated the antibody-d...
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| Veröffentlicht in: | Clinical cancer research 2007-03, Vol.13 (5), p.1552-1561 |
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| creator | KURAI, Jun CHIKUMI, Hiroki NAKAMOTO, Masaki BURIOKA, Naoto SHIMIZU, Eiji HASHIMOTO, Kiyoshi YAMAGUCHI, Kosuke YAMASAKI, Akira SAKO, Takanori TOUGE, Hirokazu MAKINO, Haruhiko TAKATA, Miyako MIYATA, Masanori |
| description | Purpose: Epidermal growth factor receptor (EGFR) is commonly overexpressed in lung cancer. Cetuximab is a chimeric mouse-human antibody
targeted against EGFR. Compared with its inhibitory properties, its immunologic mechanisms have not been well studied. In
this study, we investigated the antibody-dependent cellular cytotoxicity (ADCC) activity of cetuximab against lung cancer
cell lines.
Experimental Design: We studied the correlation between EGFR expression in lung cancer cell lines and the ADCC activity of cetuximab as well as
the influence of interleukin-2 and chemotherapy on the ADCC activity. EGFR expression was measured by a quantitative flow
cytometric analysis and immunohistochemistry. The ADCC activity was assessed by a 4-h 51 Cr release assay. Peripheral blood mononuclear cells, purified T cells, natural killer (NK) cells, and monocytes from healthy
donors or lung cancer patients were used as effector cells.
Results: Fresh peripheral blood mononuclear cells exhibited cetuximab-mediated ADCC activity against lung cancer cell lines at a low
concentration of cetuximab (0.25 μg/mL). A logarithmic correlation was observed between the number of EGFRs and ADCC activity.
Even low EGFR expression, which was weakly detectable by immunohistochemistry, was sufficient for maximum ADCC activity, and
further increases in EGFR expression on the target cells had no further effect on the ADCC activity. In addition, ADCC activity
was enhanced by interleukin-2 mainly through activation of NK cells and was less susceptible to immunosuppression by chemotherapy
than NK activity in lung cancer patients.
Conclusions: These observations suggest the importance of ADCC activity as an immunologic mechanism of cetuximab in biological therapy
for lung cancer patients. |
| doi_str_mv | 10.1158/1078-0432.CCR-06-1726 |
| format | Article |
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targeted against EGFR. Compared with its inhibitory properties, its immunologic mechanisms have not been well studied. In
this study, we investigated the antibody-dependent cellular cytotoxicity (ADCC) activity of cetuximab against lung cancer
cell lines.
Experimental Design: We studied the correlation between EGFR expression in lung cancer cell lines and the ADCC activity of cetuximab as well as
the influence of interleukin-2 and chemotherapy on the ADCC activity. EGFR expression was measured by a quantitative flow
cytometric analysis and immunohistochemistry. The ADCC activity was assessed by a 4-h 51 Cr release assay. Peripheral blood mononuclear cells, purified T cells, natural killer (NK) cells, and monocytes from healthy
donors or lung cancer patients were used as effector cells.
Results: Fresh peripheral blood mononuclear cells exhibited cetuximab-mediated ADCC activity against lung cancer cell lines at a low
concentration of cetuximab (0.25 μg/mL). A logarithmic correlation was observed between the number of EGFRs and ADCC activity.
Even low EGFR expression, which was weakly detectable by immunohistochemistry, was sufficient for maximum ADCC activity, and
further increases in EGFR expression on the target cells had no further effect on the ADCC activity. In addition, ADCC activity
was enhanced by interleukin-2 mainly through activation of NK cells and was less susceptible to immunosuppression by chemotherapy
than NK activity in lung cancer patients.
Conclusions: These observations suggest the importance of ADCC activity as an immunologic mechanism of cetuximab in biological therapy
for lung cancer patients.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-06-1726</identifier><identifier>PMID: 17332301</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>ADCC ; Adult ; Aged ; Animals ; Antibodies, Monoclonal - immunology ; Antibodies, Monoclonal - pharmacology ; Antibodies, Monoclonal, Humanized ; Antibody-Dependent Cell Cytotoxicity - drug effects ; Antineoplastic agents ; Antineoplastic Agents - immunology ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Cell Line, Tumor ; Cetuximab ; EGFR ; Female ; Flow Cytometry ; Humans ; Immunohistochemistry ; Lung Cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - immunology ; Male ; Medical sciences ; Mice ; Middle Aged ; Pharmacology. Drug treatments ; Pneumology ; Receptor, Epidermal Growth Factor - biosynthesis ; Tumors of the respiratory system and mediastinum</subject><ispartof>Clinical cancer research, 2007-03, Vol.13 (5), p.1552-1561</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-1059eddc96e9f7982a275206029624921c881e2d863b93f34dd3b9fe375cc2ee3</citedby><cites>FETCH-LOGICAL-c514t-1059eddc96e9f7982a275206029624921c881e2d863b93f34dd3b9fe375cc2ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18665019$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17332301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KURAI, Jun</creatorcontrib><creatorcontrib>CHIKUMI, Hiroki</creatorcontrib><creatorcontrib>NAKAMOTO, Masaki</creatorcontrib><creatorcontrib>BURIOKA, Naoto</creatorcontrib><creatorcontrib>SHIMIZU, Eiji</creatorcontrib><creatorcontrib>HASHIMOTO, Kiyoshi</creatorcontrib><creatorcontrib>YAMAGUCHI, Kosuke</creatorcontrib><creatorcontrib>YAMASAKI, Akira</creatorcontrib><creatorcontrib>SAKO, Takanori</creatorcontrib><creatorcontrib>TOUGE, Hirokazu</creatorcontrib><creatorcontrib>MAKINO, Haruhiko</creatorcontrib><creatorcontrib>TAKATA, Miyako</creatorcontrib><creatorcontrib>MIYATA, Masanori</creatorcontrib><title>Antibody-Dependent Cellular Cytotoxicity Mediated by Cetuximab against Lung Cancer Cell Lines</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Epidermal growth factor receptor (EGFR) is commonly overexpressed in lung cancer. Cetuximab is a chimeric mouse-human antibody
targeted against EGFR. Compared with its inhibitory properties, its immunologic mechanisms have not been well studied. In
this study, we investigated the antibody-dependent cellular cytotoxicity (ADCC) activity of cetuximab against lung cancer
cell lines.
Experimental Design: We studied the correlation between EGFR expression in lung cancer cell lines and the ADCC activity of cetuximab as well as
the influence of interleukin-2 and chemotherapy on the ADCC activity. EGFR expression was measured by a quantitative flow
cytometric analysis and immunohistochemistry. The ADCC activity was assessed by a 4-h 51 Cr release assay. Peripheral blood mononuclear cells, purified T cells, natural killer (NK) cells, and monocytes from healthy
donors or lung cancer patients were used as effector cells.
Results: Fresh peripheral blood mononuclear cells exhibited cetuximab-mediated ADCC activity against lung cancer cell lines at a low
concentration of cetuximab (0.25 μg/mL). A logarithmic correlation was observed between the number of EGFRs and ADCC activity.
Even low EGFR expression, which was weakly detectable by immunohistochemistry, was sufficient for maximum ADCC activity, and
further increases in EGFR expression on the target cells had no further effect on the ADCC activity. In addition, ADCC activity
was enhanced by interleukin-2 mainly through activation of NK cells and was less susceptible to immunosuppression by chemotherapy
than NK activity in lung cancer patients.
Conclusions: These observations suggest the importance of ADCC activity as an immunologic mechanism of cetuximab in biological therapy
for lung cancer patients.</description><subject>ADCC</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Antibodies, Monoclonal, Humanized</subject><subject>Antibody-Dependent Cell Cytotoxicity - drug effects</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - immunology</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cetuximab</subject><subject>EGFR</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lung Cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Pneumology</subject><subject>Receptor, Epidermal Growth Factor - biosynthesis</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi0Eou3CI4ByAXFJ67FjJz5WKRSkrSohOCLLsSe7RtlksR3RvH293UU9cvIcvpnxfD8h74BeAojmCmjdlLTi7LJtv5dUllAz-YKcgxB1yZkUL3P9jzkjFzH-phQqoNVrcgY154xTOCe_rsfku8kt5Q3ucXQ4pqLFYZgHE4p2SVOaHrz1aSnu0HmT0BXdkok0P_id6QqzMX6MqVjP46ZozWgxPPUXaz9ifENe9WaI-Pb0rsjPL59_tF_L9f3tt_Z6XVoBVSqBCoXOWSVR9bVqmGG1YFRSpiSrFAPbNIDMNZJ3ive8ci4XPfJaWMsQ-Yp8PM7dh-nPjDHpnY82f8OMOM1R1zRfyxT_LwhKUimyshURR9CGKcaAvd6HfHBYNFB9CEAf5OqDXJ0D0FTqQwC57_1pwdzt0D13nYxn4MMJMNGaoQ_ZmY_PXCPzflCZ-3Tktn6z_esDavtkN2BEE-xWA9dC57QZfwSAJJtt</recordid><startdate>20070301</startdate><enddate>20070301</enddate><creator>KURAI, Jun</creator><creator>CHIKUMI, Hiroki</creator><creator>NAKAMOTO, Masaki</creator><creator>BURIOKA, Naoto</creator><creator>SHIMIZU, Eiji</creator><creator>HASHIMOTO, Kiyoshi</creator><creator>YAMAGUCHI, Kosuke</creator><creator>YAMASAKI, Akira</creator><creator>SAKO, Takanori</creator><creator>TOUGE, Hirokazu</creator><creator>MAKINO, Haruhiko</creator><creator>TAKATA, Miyako</creator><creator>MIYATA, Masanori</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>H94</scope><scope>7X8</scope></search><sort><creationdate>20070301</creationdate><title>Antibody-Dependent Cellular Cytotoxicity Mediated by Cetuximab against Lung Cancer Cell Lines</title><author>KURAI, Jun ; CHIKUMI, Hiroki ; NAKAMOTO, Masaki ; BURIOKA, Naoto ; SHIMIZU, Eiji ; HASHIMOTO, Kiyoshi ; YAMAGUCHI, Kosuke ; YAMASAKI, Akira ; SAKO, Takanori ; TOUGE, Hirokazu ; MAKINO, Haruhiko ; TAKATA, Miyako ; MIYATA, Masanori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-1059eddc96e9f7982a275206029624921c881e2d863b93f34dd3b9fe375cc2ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>ADCC</topic><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Antibodies, Monoclonal, Humanized</topic><topic>Antibody-Dependent Cell Cytotoxicity - drug effects</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - immunology</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cetuximab</topic><topic>EGFR</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lung Cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Pneumology</topic><topic>Receptor, Epidermal Growth Factor - biosynthesis</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KURAI, Jun</creatorcontrib><creatorcontrib>CHIKUMI, Hiroki</creatorcontrib><creatorcontrib>NAKAMOTO, Masaki</creatorcontrib><creatorcontrib>BURIOKA, Naoto</creatorcontrib><creatorcontrib>SHIMIZU, Eiji</creatorcontrib><creatorcontrib>HASHIMOTO, Kiyoshi</creatorcontrib><creatorcontrib>YAMAGUCHI, Kosuke</creatorcontrib><creatorcontrib>YAMASAKI, Akira</creatorcontrib><creatorcontrib>SAKO, Takanori</creatorcontrib><creatorcontrib>TOUGE, Hirokazu</creatorcontrib><creatorcontrib>MAKINO, Haruhiko</creatorcontrib><creatorcontrib>TAKATA, Miyako</creatorcontrib><creatorcontrib>MIYATA, Masanori</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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KURAI, Jun</au><au>CHIKUMI, Hiroki</au><au>NAKAMOTO, Masaki</au><au>BURIOKA, Naoto</au><au>SHIMIZU, Eiji</au><au>HASHIMOTO, Kiyoshi</au><au>YAMAGUCHI, Kosuke</au><au>YAMASAKI, Akira</au><au>SAKO, Takanori</au><au>TOUGE, Hirokazu</au><au>MAKINO, Haruhiko</au><au>TAKATA, Miyako</au><au>MIYATA, Masanori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antibody-Dependent Cellular Cytotoxicity Mediated by Cetuximab against Lung Cancer Cell Lines</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2007-03-01</date><risdate>2007</risdate><volume>13</volume><issue>5</issue><spage>1552</spage><epage>1561</epage><pages>1552-1561</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Epidermal growth factor receptor (EGFR) is commonly overexpressed in lung cancer. Cetuximab is a chimeric mouse-human antibody
targeted against EGFR. Compared with its inhibitory properties, its immunologic mechanisms have not been well studied. In
this study, we investigated the antibody-dependent cellular cytotoxicity (ADCC) activity of cetuximab against lung cancer
cell lines.
Experimental Design: We studied the correlation between EGFR expression in lung cancer cell lines and the ADCC activity of cetuximab as well as
the influence of interleukin-2 and chemotherapy on the ADCC activity. EGFR expression was measured by a quantitative flow
cytometric analysis and immunohistochemistry. The ADCC activity was assessed by a 4-h 51 Cr release assay. Peripheral blood mononuclear cells, purified T cells, natural killer (NK) cells, and monocytes from healthy
donors or lung cancer patients were used as effector cells.
Results: Fresh peripheral blood mononuclear cells exhibited cetuximab-mediated ADCC activity against lung cancer cell lines at a low
concentration of cetuximab (0.25 μg/mL). A logarithmic correlation was observed between the number of EGFRs and ADCC activity.
Even low EGFR expression, which was weakly detectable by immunohistochemistry, was sufficient for maximum ADCC activity, and
further increases in EGFR expression on the target cells had no further effect on the ADCC activity. In addition, ADCC activity
was enhanced by interleukin-2 mainly through activation of NK cells and was less susceptible to immunosuppression by chemotherapy
than NK activity in lung cancer patients.
Conclusions: These observations suggest the importance of ADCC activity as an immunologic mechanism of cetuximab in biological therapy
for lung cancer patients.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>17332301</pmid><doi>10.1158/1078-0432.CCR-06-1726</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2007-03, Vol.13 (5), p.1552-1561 |
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| source | Electronic Journals Library; MEDLINE; American Association for Cancer Research; Alma/SFX Local Collection |
| subjects | ADCC Adult Aged Animals Antibodies, Monoclonal - immunology Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal, Humanized Antibody-Dependent Cell Cytotoxicity - drug effects Antineoplastic agents Antineoplastic Agents - immunology Antineoplastic Agents - pharmacology Biological and medical sciences Cell Line, Tumor Cetuximab EGFR Female Flow Cytometry Humans Immunohistochemistry Lung Cancer Lung Neoplasms - drug therapy Lung Neoplasms - immunology Male Medical sciences Mice Middle Aged Pharmacology. Drug treatments Pneumology Receptor, Epidermal Growth Factor - biosynthesis Tumors of the respiratory system and mediastinum |
| title | Antibody-Dependent Cellular Cytotoxicity Mediated by Cetuximab against Lung Cancer Cell Lines |
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