Close Association between Fas Ligand (FasL; CD95L)‐positive Tumor‐associated Macrophages and Apoptotic Cancer Cells along Invasive Margin of Colorectal Carcinoma: A Proposal on Tumor‐Host Interactions
Anti‐tumor immune responses are considered to be one of the key host reactions in human colorectal cancer, with T cells as important effector cells. For the induction of tumor‐specific immunity, processing of cancer cells and pruning of T cells by antigen‐presenting cells are important. The present...
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| Veröffentlicht in: | Cancer science 2002-03, Vol.93 (3), p.320-328 |
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| creator | Sugita, Junichi Ohtani, Haruo Mizoi, Takayuki Saito, Kazuya Shiiba, Kenichi Sasaki, Iwao Matsuno, Seiki Yagita, Hideo Miyazawa, Masaaki Nagura, Hiroshi |
| description | Anti‐tumor immune responses are considered to be one of the key host reactions in human colorectal cancer, with T cells as important effector cells. For the induction of tumor‐specific immunity, processing of cancer cells and pruning of T cells by antigen‐presenting cells are important. The present study was designed to clarify the relationship between Fas ligand (FasL; CD95L) expression and apoptotic cancer cells. Immunohistochemistry using frozen sections taken from 58 patients with colorectal cancer revealed that stromal cells composed mainly of tumor‐associated macrophages expressed FasL, leaving cancer cells negative for FasL. These macrophages were abundantly distributed along the invasive margin. In situ hybridization revealed that these macrophages as well as cancer cells expressed FasL mRNA, whereas macrophages in the normal colon mucosa rarely expressed FasL. Apoptotic cancer cells recognized by monoclonal antibody M30 CytoDEATH were localized not only in cancer cell nests, but also in the stroma along the invasive margin showing a dissociated pattern, which was particularly evident in the areas of FasL+ macrophages. Furthermore, these macrophages, phenotypically similar to dendritic cells, occasionally contained M30+ apoptotic cancer cells in the cytoplasm. Clinicopathologic analyses in 123 cases revealed 1) a positive correlation between the degree of dissociated M30+ apoptotic cancer cells and the number of macrophages along the invasive margin and 2) an inverse association between the degree of dissociated M30+ apoptotic cancer cells and the occurrence of hematogenous metastasis after surgical resection of the primary tumor. In conclusion, the present study shows the impor‐ tance of FasL+ activated macrophages as one of the host defense mechanisms against cancer cell spread in human colorectal cancer. |
| doi_str_mv | 10.1111/j.1349-7006.2002.tb02175.x |
| format | Article |
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For the induction of tumor‐specific immunity, processing of cancer cells and pruning of T cells by antigen‐presenting cells are important. The present study was designed to clarify the relationship between Fas ligand (FasL; CD95L) expression and apoptotic cancer cells. Immunohistochemistry using frozen sections taken from 58 patients with colorectal cancer revealed that stromal cells composed mainly of tumor‐associated macrophages expressed FasL, leaving cancer cells negative for FasL. These macrophages were abundantly distributed along the invasive margin. In situ hybridization revealed that these macrophages as well as cancer cells expressed FasL mRNA, whereas macrophages in the normal colon mucosa rarely expressed FasL. Apoptotic cancer cells recognized by monoclonal antibody M30 CytoDEATH were localized not only in cancer cell nests, but also in the stroma along the invasive margin showing a dissociated pattern, which was particularly evident in the areas of FasL+ macrophages. Furthermore, these macrophages, phenotypically similar to dendritic cells, occasionally contained M30+ apoptotic cancer cells in the cytoplasm. Clinicopathologic analyses in 123 cases revealed 1) a positive correlation between the degree of dissociated M30+ apoptotic cancer cells and the number of macrophages along the invasive margin and 2) an inverse association between the degree of dissociated M30+ apoptotic cancer cells and the occurrence of hematogenous metastasis after surgical resection of the primary tumor. In conclusion, the present study shows the impor‐ tance of FasL+ activated macrophages as one of the host defense mechanisms against cancer cell spread in human colorectal cancer.</description><identifier>ISSN: 0910-5050</identifier><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>EISSN: 1876-4673</identifier><identifier>DOI: 10.1111/j.1349-7006.2002.tb02175.x</identifier><identifier>PMID: 11927015</identifier><identifier>CODEN: GANNA2</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; Antigen-presenting cells ; Antigens, CD - immunology ; Antigens, CD - metabolism ; Antigens, Differentiation, Myelomonocytic - immunology ; Antigens, Differentiation, Myelomonocytic - metabolism ; Anti‐tumor immunity ; Apoptosis ; Apoptosis - physiology ; Biological and medical sciences ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Cytoplasm ; Dendritic cells ; Effector cells ; Fas ligand ; Fas Ligand Protein ; fas Receptor - immunology ; fas Receptor - metabolism ; FasL protein ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Host-tumor relations. Immunology. Biological markers ; Humans ; Hybridization ; Immunoenzyme Techniques ; Immunohistochemistry ; In Situ Hybridization ; Invasiveness ; Ligands ; Lymphocytes T ; Macrophage Activation - physiology ; Macrophages ; Macrophages - metabolism ; Male ; Medical sciences ; Membrane Glycoproteins - metabolism ; Metastases ; Microscopy, Immunoelectron ; Middle Aged ; Monoclonal antibodies ; mRNA ; Mucosa ; Neoplasm Invasiveness - genetics ; Prognosis ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Stromal cells ; Tumors ; Tumor‐associated macrophages</subject><ispartof>Cancer science, 2002-03, Vol.93 (3), p.320-328</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright John Wiley & Sons, Inc. Mar 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5880-500fe99af12d79e94a11382841c4603e10c387c8d54e36e9fa73519408a2b8ce3</citedby><cites>FETCH-LOGICAL-c5880-500fe99af12d79e94a11382841c4603e10c387c8d54e36e9fa73519408a2b8ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5926973/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5926973/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,27901,27902,45550,45551,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13640137$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11927015$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sugita, Junichi</creatorcontrib><creatorcontrib>Ohtani, Haruo</creatorcontrib><creatorcontrib>Mizoi, Takayuki</creatorcontrib><creatorcontrib>Saito, Kazuya</creatorcontrib><creatorcontrib>Shiiba, Kenichi</creatorcontrib><creatorcontrib>Sasaki, Iwao</creatorcontrib><creatorcontrib>Matsuno, Seiki</creatorcontrib><creatorcontrib>Yagita, Hideo</creatorcontrib><creatorcontrib>Miyazawa, Masaaki</creatorcontrib><creatorcontrib>Nagura, Hiroshi</creatorcontrib><title>Close Association between Fas Ligand (FasL; CD95L)‐positive Tumor‐associated Macrophages and Apoptotic Cancer Cells along Invasive Margin of Colorectal Carcinoma: A Proposal on Tumor‐Host Interactions</title><title>Cancer science</title><addtitle>Jpn J Cancer Res</addtitle><description>Anti‐tumor immune responses are considered to be one of the key host reactions in human colorectal cancer, with T cells as important effector cells. For the induction of tumor‐specific immunity, processing of cancer cells and pruning of T cells by antigen‐presenting cells are important. The present study was designed to clarify the relationship between Fas ligand (FasL; CD95L) expression and apoptotic cancer cells. Immunohistochemistry using frozen sections taken from 58 patients with colorectal cancer revealed that stromal cells composed mainly of tumor‐associated macrophages expressed FasL, leaving cancer cells negative for FasL. These macrophages were abundantly distributed along the invasive margin. In situ hybridization revealed that these macrophages as well as cancer cells expressed FasL mRNA, whereas macrophages in the normal colon mucosa rarely expressed FasL. Apoptotic cancer cells recognized by monoclonal antibody M30 CytoDEATH were localized not only in cancer cell nests, but also in the stroma along the invasive margin showing a dissociated pattern, which was particularly evident in the areas of FasL+ macrophages. Furthermore, these macrophages, phenotypically similar to dendritic cells, occasionally contained M30+ apoptotic cancer cells in the cytoplasm. Clinicopathologic analyses in 123 cases revealed 1) a positive correlation between the degree of dissociated M30+ apoptotic cancer cells and the number of macrophages along the invasive margin and 2) an inverse association between the degree of dissociated M30+ apoptotic cancer cells and the occurrence of hematogenous metastasis after surgical resection of the primary tumor. In conclusion, the present study shows the impor‐ tance of FasL+ activated macrophages as one of the host defense mechanisms against cancer cell spread in human colorectal cancer.</description><subject>Aged</subject><subject>Antigen-presenting cells</subject><subject>Antigens, CD - immunology</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation, Myelomonocytic - immunology</subject><subject>Antigens, Differentiation, Myelomonocytic - metabolism</subject><subject>Anti‐tumor immunity</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cytoplasm</subject><subject>Dendritic cells</subject><subject>Effector cells</subject><subject>Fas ligand</subject><subject>Fas Ligand Protein</subject><subject>fas Receptor - immunology</subject><subject>fas Receptor - metabolism</subject><subject>FasL protein</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Host-tumor relations. Immunology. Biological markers</subject><subject>Humans</subject><subject>Hybridization</subject><subject>Immunoenzyme Techniques</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Invasiveness</subject><subject>Ligands</subject><subject>Lymphocytes T</subject><subject>Macrophage Activation - physiology</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Metastases</subject><subject>Microscopy, Immunoelectron</subject><subject>Middle Aged</subject><subject>Monoclonal antibodies</subject><subject>mRNA</subject><subject>Mucosa</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Prognosis</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Stromal cells</subject><subject>Tumors</subject><subject>Tumor‐associated macrophages</subject><issn>0910-5050</issn><issn>1347-9032</issn><issn>1349-7006</issn><issn>1876-4673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqVUt1u0zAUjhCIlcErIAsEgosGO46TeEhIVdjYpE5wMa6tU_ekc5XamZ122x2PwJPxEDwJjhZW4A7f2Drn-z6fny9JXjCasnjerVPGczktKS3SjNIs7Rc0Y6VIbx4kk_vUw2RCJaNTQQU9SJ6EsKaUlbTIHicHjMmspExMkh916wKSWQhOG-iNs2SB_TWiJScQyNyswC7Jm_ievyf1Rynmb39--965YHqzQ3Kx3TgfAzDycUnOQXvXXcIKAxm4s851veuNJjVYjZ7U2LYx1Tq7Imd2B2EQOge_Mpa4htSudR51D20keG2s28ARmZEvUdWFGI0l_v721IU-avToQQ-1h6fJowbagM_G-zD5enJ8UZ9O558_ndWz-VSLqhpmQhuUEhqWLUuJMgfGeJVVOdN5QTkyqnlV6mopcuQFygZKLpjMaQXZotLID5MPd7rddrHBpUbbe2hV580G_K1yYNTfGWsu1crtlJBZIUseBV6PAt5dbTH0amOCjpMBi24bVMlEXGLOIvDlP8C123obm1MZl1IIXrIioo7uUHH2IXhs7kthVA2mUWs1OEMNzlCDadRoGnUTyc__bGZPHV0SAa9GAAQNbePjIk3Y43iRU8bL_VSuTYu3_1GCqmfHPKP8F2qB5Bc</recordid><startdate>200203</startdate><enddate>200203</enddate><creator>Sugita, Junichi</creator><creator>Ohtani, Haruo</creator><creator>Mizoi, Takayuki</creator><creator>Saito, Kazuya</creator><creator>Shiiba, Kenichi</creator><creator>Sasaki, Iwao</creator><creator>Matsuno, Seiki</creator><creator>Yagita, Hideo</creator><creator>Miyazawa, Masaaki</creator><creator>Nagura, Hiroshi</creator><general>Blackwell Publishing Ltd</general><general>Japanese Cancer Association</general><general>John Wiley & Sons, Inc</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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200203</creationdate><title>Close Association between Fas Ligand (FasL; CD95L)‐positive Tumor‐associated Macrophages and Apoptotic Cancer Cells along Invasive Margin of Colorectal Carcinoma: A Proposal on Tumor‐Host Interactions</title><author>Sugita, Junichi ; Ohtani, Haruo ; Mizoi, Takayuki ; Saito, Kazuya ; Shiiba, Kenichi ; Sasaki, Iwao ; Matsuno, Seiki ; Yagita, Hideo ; Miyazawa, Masaaki ; Nagura, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5880-500fe99af12d79e94a11382841c4603e10c387c8d54e36e9fa73519408a2b8ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aged</topic><topic>Antigen-presenting cells</topic><topic>Antigens, CD - immunology</topic><topic>Antigens, CD - metabolism</topic><topic>Antigens, Differentiation, Myelomonocytic - immunology</topic><topic>Antigens, Differentiation, Myelomonocytic - metabolism</topic><topic>Anti‐tumor immunity</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Cytoplasm</topic><topic>Dendritic cells</topic><topic>Effector cells</topic><topic>Fas ligand</topic><topic>Fas Ligand Protein</topic><topic>fas Receptor - immunology</topic><topic>fas Receptor - metabolism</topic><topic>FasL protein</topic><topic>Female</topic><topic>Gastroenterology. 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Anus</topic><topic>Stromal cells</topic><topic>Tumors</topic><topic>Tumor‐associated macrophages</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sugita, Junichi</creatorcontrib><creatorcontrib>Ohtani, Haruo</creatorcontrib><creatorcontrib>Mizoi, Takayuki</creatorcontrib><creatorcontrib>Saito, Kazuya</creatorcontrib><creatorcontrib>Shiiba, Kenichi</creatorcontrib><creatorcontrib>Sasaki, Iwao</creatorcontrib><creatorcontrib>Matsuno, Seiki</creatorcontrib><creatorcontrib>Yagita, Hideo</creatorcontrib><creatorcontrib>Miyazawa, Masaaki</creatorcontrib><creatorcontrib>Nagura, Hiroshi</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sugita, Junichi</au><au>Ohtani, Haruo</au><au>Mizoi, Takayuki</au><au>Saito, Kazuya</au><au>Shiiba, Kenichi</au><au>Sasaki, Iwao</au><au>Matsuno, Seiki</au><au>Yagita, Hideo</au><au>Miyazawa, Masaaki</au><au>Nagura, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Close Association between Fas Ligand (FasL; CD95L)‐positive Tumor‐associated Macrophages and Apoptotic Cancer Cells along Invasive Margin of Colorectal Carcinoma: A Proposal on Tumor‐Host Interactions</atitle><jtitle>Cancer science</jtitle><addtitle>Jpn J Cancer Res</addtitle><date>2002-03</date><risdate>2002</risdate><volume>93</volume><issue>3</issue><spage>320</spage><epage>328</epage><pages>320-328</pages><issn>0910-5050</issn><issn>1347-9032</issn><eissn>1349-7006</eissn><eissn>1876-4673</eissn><coden>GANNA2</coden><abstract>Anti‐tumor immune responses are considered to be one of the key host reactions in human colorectal cancer, with T cells as important effector cells. For the induction of tumor‐specific immunity, processing of cancer cells and pruning of T cells by antigen‐presenting cells are important. The present study was designed to clarify the relationship between Fas ligand (FasL; CD95L) expression and apoptotic cancer cells. Immunohistochemistry using frozen sections taken from 58 patients with colorectal cancer revealed that stromal cells composed mainly of tumor‐associated macrophages expressed FasL, leaving cancer cells negative for FasL. These macrophages were abundantly distributed along the invasive margin. In situ hybridization revealed that these macrophages as well as cancer cells expressed FasL mRNA, whereas macrophages in the normal colon mucosa rarely expressed FasL. Apoptotic cancer cells recognized by monoclonal antibody M30 CytoDEATH were localized not only in cancer cell nests, but also in the stroma along the invasive margin showing a dissociated pattern, which was particularly evident in the areas of FasL+ macrophages. Furthermore, these macrophages, phenotypically similar to dendritic cells, occasionally contained M30+ apoptotic cancer cells in the cytoplasm. Clinicopathologic analyses in 123 cases revealed 1) a positive correlation between the degree of dissociated M30+ apoptotic cancer cells and the number of macrophages along the invasive margin and 2) an inverse association between the degree of dissociated M30+ apoptotic cancer cells and the occurrence of hematogenous metastasis after surgical resection of the primary tumor. In conclusion, the present study shows the impor‐ tance of FasL+ activated macrophages as one of the host defense mechanisms against cancer cell spread in human colorectal cancer.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>11927015</pmid><doi>10.1111/j.1349-7006.2002.tb02175.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer science, 2002-03, Vol.93 (3), p.320-328 |
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| language | eng |
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| source | MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Aged Antigen-presenting cells Antigens, CD - immunology Antigens, CD - metabolism Antigens, Differentiation, Myelomonocytic - immunology Antigens, Differentiation, Myelomonocytic - metabolism Anti‐tumor immunity Apoptosis Apoptosis - physiology Biological and medical sciences Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Cytoplasm Dendritic cells Effector cells Fas ligand Fas Ligand Protein fas Receptor - immunology fas Receptor - metabolism FasL protein Female Gastroenterology. Liver. Pancreas. Abdomen Host-tumor relations. Immunology. Biological markers Humans Hybridization Immunoenzyme Techniques Immunohistochemistry In Situ Hybridization Invasiveness Ligands Lymphocytes T Macrophage Activation - physiology Macrophages Macrophages - metabolism Male Medical sciences Membrane Glycoproteins - metabolism Metastases Microscopy, Immunoelectron Middle Aged Monoclonal antibodies mRNA Mucosa Neoplasm Invasiveness - genetics Prognosis Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Stromal cells Tumors Tumor‐associated macrophages |
| title | Close Association between Fas Ligand (FasL; CD95L)‐positive Tumor‐associated Macrophages and Apoptotic Cancer Cells along Invasive Margin of Colorectal Carcinoma: A Proposal on Tumor‐Host Interactions |
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