Expression of Granzyme B and Perforin in Multiple Myeloma
Multiple myeloma (MM) remains an incurable disease by conventional therapy. MM tumor cells evade the immune system and can induce immunosuppression by producing immunomodifying agents such as TGF-β, FasL, vascular endothelial growth factor and Muc-1. In the present study, we show that bone marrow ce...
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| Veröffentlicht in: | Acta haematologica 2001-01, Vol.105 (3), p.125-129 |
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| container_title | Acta haematologica |
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| creator | Xagoraris, Iordanis Paterakis, George Zolota, Bassiliki Zikos, Panagiotis Maniatis, Alice Mouzaki, Athanasia |
| description | Multiple myeloma (MM) remains an incurable disease by conventional therapy. MM tumor cells evade the immune system and can induce immunosuppression by producing immunomodifying agents such as TGF-β, FasL, vascular endothelial growth factor and Muc-1. In the present study, we show that bone marrow cells from a patient suffering from MM IgG/k type, stage IIIA, when cultured, expressed granzyme B and perforin, normally expressed exlusively by cytotoxic T cells (CTLs) and natural killer (NK) cells. In addition, phenotypic analysis revealed that the cultured cells were activated antigen-presenting cells with NK targeting capacity. We propose that expression of these cytolytic enzymes may constitute an additional adoptive mechanism by the tumor cells to actively destroy the host immune effector cells. |
| doi_str_mv | 10.1159/000046553 |
| format | Article |
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MM tumor cells evade the immune system and can induce immunosuppression by producing immunomodifying agents such as TGF-β, FasL, vascular endothelial growth factor and Muc-1. In the present study, we show that bone marrow cells from a patient suffering from MM IgG/k type, stage IIIA, when cultured, expressed granzyme B and perforin, normally expressed exlusively by cytotoxic T cells (CTLs) and natural killer (NK) cells. In addition, phenotypic analysis revealed that the cultured cells were activated antigen-presenting cells with NK targeting capacity. We propose that expression of these cytolytic enzymes may constitute an additional adoptive mechanism by the tumor cells to actively destroy the host immune effector cells.</description><identifier>ISSN: 0001-5792</identifier><identifier>ISBN: 9783805572736</identifier><identifier>ISBN: 3805572735</identifier><identifier>EISSN: 1421-9662</identifier><identifier>EISBN: 3318007463</identifier><identifier>EISBN: 9783318007466</identifier><identifier>DOI: 10.1159/000046553</identifier><identifier>PMID: 11463984</identifier><identifier>CODEN: ACHAAH</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Antigen-Presenting Cells - immunology ; Apoptosis - genetics ; Biological and medical sciences ; Bone Marrow Cells - metabolism ; Bone Marrow Cells - pathology ; Gene Expression ; Genes, bcl-2 ; Granzymes ; Hematologic and hematopoietic diseases ; Humans ; Immunophenotyping ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - immunology ; Membrane Glycoproteins - metabolism ; Middle Aged ; Multiple Myeloma - genetics ; Multiple Myeloma - metabolism ; Multiple Myeloma - pathology ; Perforin ; Pore Forming Cytotoxic Proteins ; RNA, Messenger - biosynthesis ; Serine Endopeptidases - genetics ; Serine Endopeptidases - immunology ; Serine Endopeptidases - metabolism ; Time Factors ; Tumor Cells, Cultured</subject><ispartof>Acta haematologica, 2001-01, Vol.105 (3), p.125-129</ispartof><rights>2001 S. Karger AG, Basel</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2001 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c358t-5f03ec579f9892471630668cab0e1a38cbf803ec39bb2f07df9e547eb173ab763</citedby><cites>FETCH-LOGICAL-c358t-5f03ec579f9892471630668cab0e1a38cbf803ec39bb2f07df9e547eb173ab763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,2423,23909,23910,25118,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14084307$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11463984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xagoraris, Iordanis</creatorcontrib><creatorcontrib>Paterakis, George</creatorcontrib><creatorcontrib>Zolota, Bassiliki</creatorcontrib><creatorcontrib>Zikos, Panagiotis</creatorcontrib><creatorcontrib>Maniatis, Alice</creatorcontrib><creatorcontrib>Mouzaki, Athanasia</creatorcontrib><title>Expression of Granzyme B and Perforin in Multiple Myeloma</title><title>Acta haematologica</title><addtitle>Acta Haematol</addtitle><description>Multiple myeloma (MM) remains an incurable disease by conventional therapy. MM tumor cells evade the immune system and can induce immunosuppression by producing immunomodifying agents such as TGF-β, FasL, vascular endothelial growth factor and Muc-1. In the present study, we show that bone marrow cells from a patient suffering from MM IgG/k type, stage IIIA, when cultured, expressed granzyme B and perforin, normally expressed exlusively by cytotoxic T cells (CTLs) and natural killer (NK) cells. In addition, phenotypic analysis revealed that the cultured cells were activated antigen-presenting cells with NK targeting capacity. We propose that expression of these cytolytic enzymes may constitute an additional adoptive mechanism by the tumor cells to actively destroy the host immune effector cells.</description><subject>Antigen-Presenting Cells - immunology</subject><subject>Apoptosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Cells - pathology</subject><subject>Gene Expression</subject><subject>Genes, bcl-2</subject><subject>Granzymes</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunophenotyping</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Middle Aged</subject><subject>Multiple Myeloma - genetics</subject><subject>Multiple Myeloma - metabolism</subject><subject>Multiple Myeloma - pathology</subject><subject>Perforin</subject><subject>Pore Forming Cytotoxic Proteins</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Serine Endopeptidases - genetics</subject><subject>Serine Endopeptidases - immunology</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Time Factors</subject><subject>Tumor Cells, Cultured</subject><issn>0001-5792</issn><issn>1421-9662</issn><isbn>9783805572736</isbn><isbn>3805572735</isbn><isbn>3318007463</isbn><isbn>9783318007466</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0MtLwzAcB_D4wj3cwbMgRVDwUE2a5nWcY27Chh70XNI0kWpfJis4_3ozV7aLIRBCPr9ffnwBOEfwDiEi7qFfMSUEH4ABxohDyGKKD0EfxREKBaXRERgJxjGHhLCIYXoM-r4GhYSJqAcGzn34m38Qp6CHkC8WPO4DMf1urHYur6ugNsHMyupnXergIZBVFrxoa2qbV4Hfy7ZY5U2hg-VaF3Upz8CJkYXTo-4cgrfH6etkHi6eZ0-T8SJUmPBVSAzEWvkhjOAiihmiGFLKlUyhRhJzlRq-EVikaWQgy4zQJGY6RQzLlFE8BDfbvo2tv1rtVkmZO6WLQla6bl3CEEQ0ipCHt1uobO2c1SZpbF5Ku04QTDYhJrsQvb3smrZpqbO97ILx4LoD0ilZGJ-Lyt3exdAjyLy72rpPad-13YHxfPz3U9JkxqOLf9F2ll9An4bk</recordid><startdate>20010101</startdate><enddate>20010101</enddate><creator>Xagoraris, Iordanis</creator><creator>Paterakis, George</creator><creator>Zolota, Bassiliki</creator><creator>Zikos, Panagiotis</creator><creator>Maniatis, Alice</creator><creator>Mouzaki, Athanasia</creator><general>Karger</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>7X8</scope></search><sort><creationdate>20010101</creationdate><title>Expression of Granzyme B and Perforin in Multiple Myeloma</title><author>Xagoraris, Iordanis ; Paterakis, George ; Zolota, Bassiliki ; Zikos, Panagiotis ; Maniatis, Alice ; Mouzaki, Athanasia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-5f03ec579f9892471630668cab0e1a38cbf803ec39bb2f07df9e547eb173ab763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Antigen-Presenting Cells - immunology</topic><topic>Apoptosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone Marrow Cells - pathology</topic><topic>Gene Expression</topic><topic>Genes, bcl-2</topic><topic>Granzymes</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunophenotyping</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - immunology</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Middle Aged</topic><topic>Multiple Myeloma - genetics</topic><topic>Multiple Myeloma - metabolism</topic><topic>Multiple Myeloma - pathology</topic><topic>Perforin</topic><topic>Pore Forming Cytotoxic Proteins</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Serine Endopeptidases - genetics</topic><topic>Serine Endopeptidases - immunology</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Time Factors</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xagoraris, Iordanis</creatorcontrib><creatorcontrib>Paterakis, George</creatorcontrib><creatorcontrib>Zolota, Bassiliki</creatorcontrib><creatorcontrib>Zikos, Panagiotis</creatorcontrib><creatorcontrib>Maniatis, Alice</creatorcontrib><creatorcontrib>Mouzaki, Athanasia</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>MEDLINE - Academic</collection><jtitle>Acta haematologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xagoraris, Iordanis</au><au>Paterakis, George</au><au>Zolota, Bassiliki</au><au>Zikos, Panagiotis</au><au>Maniatis, Alice</au><au>Mouzaki, Athanasia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Granzyme B and Perforin in Multiple Myeloma</atitle><jtitle>Acta haematologica</jtitle><addtitle>Acta Haematol</addtitle><date>2001-01-01</date><risdate>2001</risdate><volume>105</volume><issue>3</issue><spage>125</spage><epage>129</epage><pages>125-129</pages><issn>0001-5792</issn><eissn>1421-9662</eissn><isbn>9783805572736</isbn><isbn>3805572735</isbn><eisbn>3318007463</eisbn><eisbn>9783318007466</eisbn><coden>ACHAAH</coden><abstract>Multiple myeloma (MM) remains an incurable disease by conventional therapy. MM tumor cells evade the immune system and can induce immunosuppression by producing immunomodifying agents such as TGF-β, FasL, vascular endothelial growth factor and Muc-1. In the present study, we show that bone marrow cells from a patient suffering from MM IgG/k type, stage IIIA, when cultured, expressed granzyme B and perforin, normally expressed exlusively by cytotoxic T cells (CTLs) and natural killer (NK) cells. In addition, phenotypic analysis revealed that the cultured cells were activated antigen-presenting cells with NK targeting capacity. We propose that expression of these cytolytic enzymes may constitute an additional adoptive mechanism by the tumor cells to actively destroy the host immune effector cells.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>11463984</pmid><doi>10.1159/000046553</doi><tpages>5</tpages></addata></record> |
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| subjects | Antigen-Presenting Cells - immunology Apoptosis - genetics Biological and medical sciences Bone Marrow Cells - metabolism Bone Marrow Cells - pathology Gene Expression Genes, bcl-2 Granzymes Hematologic and hematopoietic diseases Humans Immunophenotyping Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Membrane Glycoproteins - genetics Membrane Glycoproteins - immunology Membrane Glycoproteins - metabolism Middle Aged Multiple Myeloma - genetics Multiple Myeloma - metabolism Multiple Myeloma - pathology Perforin Pore Forming Cytotoxic Proteins RNA, Messenger - biosynthesis Serine Endopeptidases - genetics Serine Endopeptidases - immunology Serine Endopeptidases - metabolism Time Factors Tumor Cells, Cultured |
| title | Expression of Granzyme B and Perforin in Multiple Myeloma |
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