Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model
The negative signal provided by interactions of programmed death-1 (PD-1) and its ligands, B7-H1 and B7-DC, has been suggested to play an important role in tumor evasion from host immunity. Pancreas cancer patients with B7-H1 expression have a poor prognosis. B7-H1 blocking has been shown to inhibit...
Gespeichert in:
| Veröffentlicht in: | International journal of oncology 2009-10, Vol.35 (4), p.741-749 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 749 |
|---|---|
| container_issue | 4 |
| container_start_page | 741 |
| container_title | International journal of oncology |
| container_volume | 35 |
| creator | OKUDAIRA, Keisuke HOKARI, Ryota YAGITA, Hideo MIURA, Soichiro TSUZUKI, Yoshikazu OKADA, Yoshikiyo KOMOTO, Shunsuke WATANABE, Chikako KURIHARA, Chie KAWAGUCHI, Atsushi NAGAO, Shigeaki AZUMA, Miyuki |
| description | The negative signal provided by interactions of programmed death-1 (PD-1) and its ligands, B7-H1 and B7-DC, has been suggested to play an important role in tumor evasion from host immunity. Pancreas cancer patients with B7-H1 expression have a poor prognosis. B7-H1 blocking has been shown to inhibit the development of a subcutaneous tumor from a pancreas cancer cell line. In this study, we investigated the effects of B7-DC as well as B7-H1 blockade in vivo in a murine pancreatic cancer model. Pancreatic cancer cells (Panc02) were inoculated in the pancreas of C57BL/6 mice. Five weeks later, tumor sizes were measured and the mice bearing appropriate size of tumors received the following treatments. Blocking antibodies against B7-H1 or B7-DC (200 microg) were administered 3 times/week for 3 weeks. Cells infiltrating the tumors were characterized by immunohistochemistry. Effects of antibodies on cytokine and FoxP3 expression were examined by quantitative RT-PCR. In vitro cultured Panc02 cells expressed B7-H1 upon IFN-gamma stimulation. However, expression of B7-H1 and B7-DC was found mainly on CD45-positive infiltrating cells and rarely on cancer cells in vivo. Treatment with both antibodies significantly decreased tumor growth in vivo. B7-DC blockade decreased the levels of IL-10 and FoxP3, suggesting that regulatory systems are mainly inhibited at the tumor site. B7-H1 blockade increased the levels of IFN-gamma and FoxP3. Collectively, blocking of B7-H1 or B7-DC efficiently induced regression of pre-established pancreatic cancers by up-regulating IFN-gamma production and down-regulating IL-10 production at the tumor site. |
| doi_str_mv | 10.3892/ijo_00000387 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_755138058</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>755138058</sourcerecordid><originalsourceid>FETCH-LOGICAL-c358t-d76d3381c6e78f342d62e137e54813af1aa300af3421da3bf9de4a18754dbc803</originalsourceid><addsrcrecordid>eNpNkEtLxDAUhYMozji6cy3ZiBuruUnbpEtnfIww4EY3bkomuYGOfYxJu_Dfm2JRQyCHnI_DvYeQc2A3QhX8ttp1JRuPUPKAzEEWkPCUi8OoGRRJnopiRk5C2DHGs4zBMZlBIXlaAJuT92XdmQ9tkXaOLmWyBtr5UdyvaNXawWCguo23r5J-aKKHzqHpo0k1bbohIN3r1njUfWWoiRJ9_LdYn5Ijp-uAZ9O7IG-PD6-rdbJ5eXpe3W0SIzLVJ1bmVggFJkepnEi5zTmCkJilCoR2oLVgTI8OWC22rrCYalAyS-3WKCYW5Oond--7zwFDXzZVMFjXusU4XymzDIRimYrk9Q9pfBeCR1fufdVo_1UCK8cyy_9lRvxiCh62Ddo_eGovApcToIPRtfNx-yr8chwKJtM8F99Fa3px</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>755138058</pqid></control><display><type>article</type><title>Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>OKUDAIRA, Keisuke ; HOKARI, Ryota ; YAGITA, Hideo ; MIURA, Soichiro ; TSUZUKI, Yoshikazu ; OKADA, Yoshikiyo ; KOMOTO, Shunsuke ; WATANABE, Chikako ; KURIHARA, Chie ; KAWAGUCHI, Atsushi ; NAGAO, Shigeaki ; AZUMA, Miyuki</creator><creatorcontrib>OKUDAIRA, Keisuke ; HOKARI, Ryota ; YAGITA, Hideo ; MIURA, Soichiro ; TSUZUKI, Yoshikazu ; OKADA, Yoshikiyo ; KOMOTO, Shunsuke ; WATANABE, Chikako ; KURIHARA, Chie ; KAWAGUCHI, Atsushi ; NAGAO, Shigeaki ; AZUMA, Miyuki</creatorcontrib><description>The negative signal provided by interactions of programmed death-1 (PD-1) and its ligands, B7-H1 and B7-DC, has been suggested to play an important role in tumor evasion from host immunity. Pancreas cancer patients with B7-H1 expression have a poor prognosis. B7-H1 blocking has been shown to inhibit the development of a subcutaneous tumor from a pancreas cancer cell line. In this study, we investigated the effects of B7-DC as well as B7-H1 blockade in vivo in a murine pancreatic cancer model. Pancreatic cancer cells (Panc02) were inoculated in the pancreas of C57BL/6 mice. Five weeks later, tumor sizes were measured and the mice bearing appropriate size of tumors received the following treatments. Blocking antibodies against B7-H1 or B7-DC (200 microg) were administered 3 times/week for 3 weeks. Cells infiltrating the tumors were characterized by immunohistochemistry. Effects of antibodies on cytokine and FoxP3 expression were examined by quantitative RT-PCR. In vitro cultured Panc02 cells expressed B7-H1 upon IFN-gamma stimulation. However, expression of B7-H1 and B7-DC was found mainly on CD45-positive infiltrating cells and rarely on cancer cells in vivo. Treatment with both antibodies significantly decreased tumor growth in vivo. B7-DC blockade decreased the levels of IL-10 and FoxP3, suggesting that regulatory systems are mainly inhibited at the tumor site. B7-H1 blockade increased the levels of IFN-gamma and FoxP3. Collectively, blocking of B7-H1 or B7-DC efficiently induced regression of pre-established pancreatic cancers by up-regulating IFN-gamma production and down-regulating IL-10 production at the tumor site.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo_00000387</identifier><identifier>PMID: 19724910</identifier><language>eng</language><publisher>Athens: Editorial Academy of the International Journal of Oncology</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - immunology ; Adenocarcinoma - pathology ; Animals ; Antibodies, Blocking - pharmacology ; Antigens, CD - analysis ; Antigens, Differentiation - immunology ; Antigens, Differentiation, Myelomonocytic - analysis ; Antineoplastic Agents - pharmacology ; B7-1 Antigen - drug effects ; B7-1 Antigen - immunology ; B7-H1 Antigen ; Biological and medical sciences ; CD11b Antigen - analysis ; CD4 Antigens - analysis ; CD8 Antigens - analysis ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Forkhead Transcription Factors - genetics ; Gastroenterology. Liver. Pancreas. Abdomen ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-10 - genetics ; Leukocyte Common Antigens - analysis ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Lymphocytes, Tumor-Infiltrating - drug effects ; Lymphocytes, Tumor-Infiltrating - immunology ; Male ; Medical sciences ; Membrane Glycoproteins - antagonists & inhibitors ; Membrane Glycoproteins - immunology ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - immunology ; Pancreatic Neoplasms - pathology ; Peptides - antagonists & inhibitors ; Peptides - immunology ; Programmed Cell Death 1 Ligand 2 Protein ; Programmed Cell Death 1 Receptor ; RNA, Messenger - metabolism ; T-Lymphocytes, Regulatory - drug effects ; T-Lymphocytes, Regulatory - immunology ; Tumor Escape - drug effects ; Tumors</subject><ispartof>International journal of oncology, 2009-10, Vol.35 (4), p.741-749</ispartof><rights>2009 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c358t-d76d3381c6e78f342d62e137e54813af1aa300af3421da3bf9de4a18754dbc803</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21907466$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19724910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OKUDAIRA, Keisuke</creatorcontrib><creatorcontrib>HOKARI, Ryota</creatorcontrib><creatorcontrib>YAGITA, Hideo</creatorcontrib><creatorcontrib>MIURA, Soichiro</creatorcontrib><creatorcontrib>TSUZUKI, Yoshikazu</creatorcontrib><creatorcontrib>OKADA, Yoshikiyo</creatorcontrib><creatorcontrib>KOMOTO, Shunsuke</creatorcontrib><creatorcontrib>WATANABE, Chikako</creatorcontrib><creatorcontrib>KURIHARA, Chie</creatorcontrib><creatorcontrib>KAWAGUCHI, Atsushi</creatorcontrib><creatorcontrib>NAGAO, Shigeaki</creatorcontrib><creatorcontrib>AZUMA, Miyuki</creatorcontrib><title>Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>The negative signal provided by interactions of programmed death-1 (PD-1) and its ligands, B7-H1 and B7-DC, has been suggested to play an important role in tumor evasion from host immunity. Pancreas cancer patients with B7-H1 expression have a poor prognosis. B7-H1 blocking has been shown to inhibit the development of a subcutaneous tumor from a pancreas cancer cell line. In this study, we investigated the effects of B7-DC as well as B7-H1 blockade in vivo in a murine pancreatic cancer model. Pancreatic cancer cells (Panc02) were inoculated in the pancreas of C57BL/6 mice. Five weeks later, tumor sizes were measured and the mice bearing appropriate size of tumors received the following treatments. Blocking antibodies against B7-H1 or B7-DC (200 microg) were administered 3 times/week for 3 weeks. Cells infiltrating the tumors were characterized by immunohistochemistry. Effects of antibodies on cytokine and FoxP3 expression were examined by quantitative RT-PCR. In vitro cultured Panc02 cells expressed B7-H1 upon IFN-gamma stimulation. However, expression of B7-H1 and B7-DC was found mainly on CD45-positive infiltrating cells and rarely on cancer cells in vivo. Treatment with both antibodies significantly decreased tumor growth in vivo. B7-DC blockade decreased the levels of IL-10 and FoxP3, suggesting that regulatory systems are mainly inhibited at the tumor site. B7-H1 blockade increased the levels of IFN-gamma and FoxP3. Collectively, blocking of B7-H1 or B7-DC efficiently induced regression of pre-established pancreatic cancers by up-regulating IFN-gamma production and down-regulating IL-10 production at the tumor site.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - immunology</subject><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Antibodies, Blocking - pharmacology</subject><subject>Antigens, CD - analysis</subject><subject>Antigens, Differentiation - immunology</subject><subject>Antigens, Differentiation, Myelomonocytic - analysis</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>B7-1 Antigen - drug effects</subject><subject>B7-1 Antigen - immunology</subject><subject>B7-H1 Antigen</subject><subject>Biological and medical sciences</subject><subject>CD11b Antigen - analysis</subject><subject>CD4 Antigens - analysis</subject><subject>CD8 Antigens - analysis</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-10 - genetics</subject><subject>Leukocyte Common Antigens - analysis</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Lymphocytes, Tumor-Infiltrating - drug effects</subject><subject>Lymphocytes, Tumor-Infiltrating - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - antagonists & inhibitors</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - immunology</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Peptides - antagonists & inhibitors</subject><subject>Peptides - immunology</subject><subject>Programmed Cell Death 1 Ligand 2 Protein</subject><subject>Programmed Cell Death 1 Receptor</subject><subject>RNA, Messenger - metabolism</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Tumor Escape - drug effects</subject><subject>Tumors</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkEtLxDAUhYMozji6cy3ZiBuruUnbpEtnfIww4EY3bkomuYGOfYxJu_Dfm2JRQyCHnI_DvYeQc2A3QhX8ttp1JRuPUPKAzEEWkPCUi8OoGRRJnopiRk5C2DHGs4zBMZlBIXlaAJuT92XdmQ9tkXaOLmWyBtr5UdyvaNXawWCguo23r5J-aKKHzqHpo0k1bbohIN3r1njUfWWoiRJ9_LdYn5Ijp-uAZ9O7IG-PD6-rdbJ5eXpe3W0SIzLVJ1bmVggFJkepnEi5zTmCkJilCoR2oLVgTI8OWC22rrCYalAyS-3WKCYW5Oond--7zwFDXzZVMFjXusU4XymzDIRimYrk9Q9pfBeCR1fufdVo_1UCK8cyy_9lRvxiCh62Ddo_eGovApcToIPRtfNx-yr8chwKJtM8F99Fa3px</recordid><startdate>20091001</startdate><enddate>20091001</enddate><creator>OKUDAIRA, Keisuke</creator><creator>HOKARI, Ryota</creator><creator>YAGITA, Hideo</creator><creator>MIURA, Soichiro</creator><creator>TSUZUKI, Yoshikazu</creator><creator>OKADA, Yoshikiyo</creator><creator>KOMOTO, Shunsuke</creator><creator>WATANABE, Chikako</creator><creator>KURIHARA, Chie</creator><creator>KAWAGUCHI, Atsushi</creator><creator>NAGAO, Shigeaki</creator><creator>AZUMA, Miyuki</creator><general>Editorial Academy of the International Journal of Oncology</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>7TO</scope><scope>H94</scope></search><sort><creationdate>20091001</creationdate><title>Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model</title><author>OKUDAIRA, Keisuke ; HOKARI, Ryota ; YAGITA, Hideo ; MIURA, Soichiro ; TSUZUKI, Yoshikazu ; OKADA, Yoshikiyo ; KOMOTO, Shunsuke ; WATANABE, Chikako ; KURIHARA, Chie ; KAWAGUCHI, Atsushi ; NAGAO, Shigeaki ; AZUMA, Miyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-d76d3381c6e78f342d62e137e54813af1aa300af3421da3bf9de4a18754dbc803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - immunology</topic><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Antibodies, Blocking - pharmacology</topic><topic>Antigens, CD - analysis</topic><topic>Antigens, Differentiation - immunology</topic><topic>Antigens, Differentiation, Myelomonocytic - analysis</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>B7-1 Antigen - drug effects</topic><topic>B7-1 Antigen - immunology</topic><topic>B7-H1 Antigen</topic><topic>Biological and medical sciences</topic><topic>CD11b Antigen - analysis</topic><topic>CD4 Antigens - analysis</topic><topic>CD8 Antigens - analysis</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-10 - genetics</topic><topic>Leukocyte Common Antigens - analysis</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Lymphocytes, Tumor-Infiltrating - drug effects</topic><topic>Lymphocytes, Tumor-Infiltrating - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - antagonists & inhibitors</topic><topic>Membrane Glycoproteins - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - immunology</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Peptides - antagonists & inhibitors</topic><topic>Peptides - immunology</topic><topic>Programmed Cell Death 1 Ligand 2 Protein</topic><topic>Programmed Cell Death 1 Receptor</topic><topic>RNA, Messenger - metabolism</topic><topic>T-Lymphocytes, Regulatory - drug effects</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Tumor Escape - drug effects</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>OKUDAIRA, Keisuke</creatorcontrib><creatorcontrib>HOKARI, Ryota</creatorcontrib><creatorcontrib>YAGITA, Hideo</creatorcontrib><creatorcontrib>MIURA, Soichiro</creatorcontrib><creatorcontrib>TSUZUKI, Yoshikazu</creatorcontrib><creatorcontrib>OKADA, Yoshikiyo</creatorcontrib><creatorcontrib>KOMOTO, Shunsuke</creatorcontrib><creatorcontrib>WATANABE, Chikako</creatorcontrib><creatorcontrib>KURIHARA, Chie</creatorcontrib><creatorcontrib>KAWAGUCHI, Atsushi</creatorcontrib><creatorcontrib>NAGAO, Shigeaki</creatorcontrib><creatorcontrib>AZUMA, Miyuki</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OKUDAIRA, Keisuke</au><au>HOKARI, Ryota</au><au>YAGITA, Hideo</au><au>MIURA, Soichiro</au><au>TSUZUKI, Yoshikazu</au><au>OKADA, Yoshikiyo</au><au>KOMOTO, Shunsuke</au><au>WATANABE, Chikako</au><au>KURIHARA, Chie</au><au>KAWAGUCHI, Atsushi</au><au>NAGAO, Shigeaki</au><au>AZUMA, Miyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2009-10-01</date><risdate>2009</risdate><volume>35</volume><issue>4</issue><spage>741</spage><epage>749</epage><pages>741-749</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>The negative signal provided by interactions of programmed death-1 (PD-1) and its ligands, B7-H1 and B7-DC, has been suggested to play an important role in tumor evasion from host immunity. Pancreas cancer patients with B7-H1 expression have a poor prognosis. B7-H1 blocking has been shown to inhibit the development of a subcutaneous tumor from a pancreas cancer cell line. In this study, we investigated the effects of B7-DC as well as B7-H1 blockade in vivo in a murine pancreatic cancer model. Pancreatic cancer cells (Panc02) were inoculated in the pancreas of C57BL/6 mice. Five weeks later, tumor sizes were measured and the mice bearing appropriate size of tumors received the following treatments. Blocking antibodies against B7-H1 or B7-DC (200 microg) were administered 3 times/week for 3 weeks. Cells infiltrating the tumors were characterized by immunohistochemistry. Effects of antibodies on cytokine and FoxP3 expression were examined by quantitative RT-PCR. In vitro cultured Panc02 cells expressed B7-H1 upon IFN-gamma stimulation. However, expression of B7-H1 and B7-DC was found mainly on CD45-positive infiltrating cells and rarely on cancer cells in vivo. Treatment with both antibodies significantly decreased tumor growth in vivo. B7-DC blockade decreased the levels of IL-10 and FoxP3, suggesting that regulatory systems are mainly inhibited at the tumor site. B7-H1 blockade increased the levels of IFN-gamma and FoxP3. Collectively, blocking of B7-H1 or B7-DC efficiently induced regression of pre-established pancreatic cancers by up-regulating IFN-gamma production and down-regulating IL-10 production at the tumor site.</abstract><cop>Athens</cop><pub>Editorial Academy of the International Journal of Oncology</pub><pmid>19724910</pmid><doi>10.3892/ijo_00000387</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1019-6439 |
| ispartof | International journal of oncology, 2009-10, Vol.35 (4), p.741-749 |
| issn | 1019-6439 1791-2423 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_755138058 |
| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - immunology Adenocarcinoma - pathology Animals Antibodies, Blocking - pharmacology Antigens, CD - analysis Antigens, Differentiation - immunology Antigens, Differentiation, Myelomonocytic - analysis Antineoplastic Agents - pharmacology B7-1 Antigen - drug effects B7-1 Antigen - immunology B7-H1 Antigen Biological and medical sciences CD11b Antigen - analysis CD4 Antigens - analysis CD8 Antigens - analysis Cell Line, Tumor Cell Proliferation - drug effects Forkhead Transcription Factors - genetics Gastroenterology. Liver. Pancreas. Abdomen Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-10 - genetics Leukocyte Common Antigens - analysis Liver. Biliary tract. Portal circulation. Exocrine pancreas Lymphocytes, Tumor-Infiltrating - drug effects Lymphocytes, Tumor-Infiltrating - immunology Male Medical sciences Membrane Glycoproteins - antagonists & inhibitors Membrane Glycoproteins - immunology Mice Mice, Inbred C57BL Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - immunology Pancreatic Neoplasms - pathology Peptides - antagonists & inhibitors Peptides - immunology Programmed Cell Death 1 Ligand 2 Protein Programmed Cell Death 1 Receptor RNA, Messenger - metabolism T-Lymphocytes, Regulatory - drug effects T-Lymphocytes, Regulatory - immunology Tumor Escape - drug effects Tumors |
| title | Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T18%3A02%3A02IST&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=Blockade%20of%20B7-H1%20or%20B7-DC%20induces%20an%20anti-tumor%20effect%20in%20a%20mouse%20pancreatic%20cancer%20model&rft.jtitle=International%20journal%20of%20oncology&rft.au=OKUDAIRA,%20Keisuke&rft.date=2009-10-01&rft.volume=35&rft.issue=4&rft.spage=741&rft.epage=749&rft.pages=741-749&rft.issn=1019-6439&rft.eissn=1791-2423&rft_id=info:doi/10.3892/ijo_00000387&rft_dat=%3Cproquest_cross%3E755138058%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=755138058&rft_id=info:pmid/19724910&rfr_iscdi=true |