Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control
Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass...
Gespeichert in:
| Veröffentlicht in: | The Journal of clinical investigation 1989-08, Vol.84 (2), p.451-457 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 457 |
|---|---|
| container_issue | 2 |
| container_start_page | 451 |
| container_title | The Journal of clinical investigation |
| container_volume | 84 |
| creator | OSTER, W CICCO, N. A KLEIN, H HIRANO, T KISHIMOTO, T LINDEMANN, A MERTELSMANN, R. H HERRMANN, F |
| description | Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6, TNF-alpha, and IL-1 in growth control of AML were investigated in vitro. We show that a substantial proportion of AML cells produce IL-6, TNF-alpha, and IL-1-beta and use these mediators to stimulate their growth by disparate mechanisms: IL-6 acts as a costimulator to enhance CSF-induced clonogenicity of AML blasts. TNF-alpha induces CSF production by endothelial cells and may therefore provide a paracrine loop to support leukemia growth. |
| doi_str_mv | 10.1172/jci114186 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_548903</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>79136466</sourcerecordid><originalsourceid>FETCH-LOGICAL-c495t-c20bb179d316f10223fb6de87d1af8d9a687ad122deba3b1aafddcaf7636bc083</originalsourceid><addsrcrecordid>eNqFks-O0zAQxi0EWsrCgQdA8gEhIW3AYyeOc-CAKv4sWgkOcI4m9qT1ksTFdkB9PZ6MlFYVe-Jkjb7fzDcaf4w9BfEKoJavb60HKMHoe2wFVWUKI5W5z1ZCSCiaWpmH7FFKt0JAWVblBbuQtTFQqxX7_QVj9tbvMPsw8dDzvCVu9zl89xMl7qdMcaB5qbi-4nkeQ-QT2RiST7xHm0MscNht8Yrj5O7wUHSUkaeFpkyOd3uOds7Exz0NYUNTmBM_sDR65N2AKR8MOc452LjY_524w4jH6oxuYviVt9yGKccwPGYPehwSPTm9l-zb-3df1x-Lm88frtdvbwpbNlUurBRdB3XjFOgehJSq77QjUzvA3rgGtanRgZSOOlQdIPbOWexrrXRnhVGX7M1x7m7uRnKWFncc2l30I8Z9G9C3d5XJb9tN-NlWpWmEWvpfnPpj-DFTyu3ok6VhwImWS7R1A0qXWv8XhEo2IHS5gC-P4OE7UqT-vAyI9hCM9tP6-hiMhX327_Zn8pSERX9-0jFZHPqIk_XpjNUKDMhK_QFAucef</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15291064</pqid></control><display><type>article</type><title>Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>OSTER, W ; CICCO, N. A ; KLEIN, H ; HIRANO, T ; KISHIMOTO, T ; LINDEMANN, A ; MERTELSMANN, R. H ; HERRMANN, F</creator><creatorcontrib>OSTER, W ; CICCO, N. A ; KLEIN, H ; HIRANO, T ; KISHIMOTO, T ; LINDEMANN, A ; MERTELSMANN, R. H ; HERRMANN, F</creatorcontrib><description>Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6, TNF-alpha, and IL-1 in growth control of AML were investigated in vitro. We show that a substantial proportion of AML cells produce IL-6, TNF-alpha, and IL-1-beta and use these mediators to stimulate their growth by disparate mechanisms: IL-6 acts as a costimulator to enhance CSF-induced clonogenicity of AML blasts. TNF-alpha induces CSF production by endothelial cells and may therefore provide a paracrine loop to support leukemia growth.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/jci114186</identifier><identifier>PMID: 2788173</identifier><identifier>CODEN: JCINAO</identifier><language>eng</language><publisher>Ann Arbor, MI: American Society for Clinical Investigation</publisher><subject>Biological and medical sciences ; Colony-Stimulating Factors - biosynthesis ; Colony-Stimulating Factors - genetics ; Hematologic and hematopoietic diseases ; Humans ; Interleukin-1 - genetics ; Interleukin-1 - physiology ; Interleukin-6 ; Interleukins - genetics ; Interleukins - physiology ; Leukemia, Myeloid, Acute - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Neoplastic Stem Cells - pathology ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - physiology</subject><ispartof>The Journal of clinical investigation, 1989-08, Vol.84 (2), p.451-457</ispartof><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-c20bb179d316f10223fb6de87d1af8d9a687ad122deba3b1aafddcaf7636bc083</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC548903/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC548903/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7318125$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2788173$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OSTER, W</creatorcontrib><creatorcontrib>CICCO, N. A</creatorcontrib><creatorcontrib>KLEIN, H</creatorcontrib><creatorcontrib>HIRANO, T</creatorcontrib><creatorcontrib>KISHIMOTO, T</creatorcontrib><creatorcontrib>LINDEMANN, A</creatorcontrib><creatorcontrib>MERTELSMANN, R. H</creatorcontrib><creatorcontrib>HERRMANN, F</creatorcontrib><title>Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6, TNF-alpha, and IL-1 in growth control of AML were investigated in vitro. We show that a substantial proportion of AML cells produce IL-6, TNF-alpha, and IL-1-beta and use these mediators to stimulate their growth by disparate mechanisms: IL-6 acts as a costimulator to enhance CSF-induced clonogenicity of AML blasts. TNF-alpha induces CSF production by endothelial cells and may therefore provide a paracrine loop to support leukemia growth.</description><subject>Biological and medical sciences</subject><subject>Colony-Stimulating Factors - biosynthesis</subject><subject>Colony-Stimulating Factors - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Interleukin-1 - genetics</subject><subject>Interleukin-1 - physiology</subject><subject>Interleukin-6</subject><subject>Interleukins - genetics</subject><subject>Interleukins - physiology</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks-O0zAQxi0EWsrCgQdA8gEhIW3AYyeOc-CAKv4sWgkOcI4m9qT1ksTFdkB9PZ6MlFYVe-Jkjb7fzDcaf4w9BfEKoJavb60HKMHoe2wFVWUKI5W5z1ZCSCiaWpmH7FFKt0JAWVblBbuQtTFQqxX7_QVj9tbvMPsw8dDzvCVu9zl89xMl7qdMcaB5qbi-4nkeQ-QT2RiST7xHm0MscNht8Yrj5O7wUHSUkaeFpkyOd3uOds7Exz0NYUNTmBM_sDR65N2AKR8MOc452LjY_524w4jH6oxuYviVt9yGKccwPGYPehwSPTm9l-zb-3df1x-Lm88frtdvbwpbNlUurBRdB3XjFOgehJSq77QjUzvA3rgGtanRgZSOOlQdIPbOWexrrXRnhVGX7M1x7m7uRnKWFncc2l30I8Z9G9C3d5XJb9tN-NlWpWmEWvpfnPpj-DFTyu3ok6VhwImWS7R1A0qXWv8XhEo2IHS5gC-P4OE7UqT-vAyI9hCM9tP6-hiMhX327_Zn8pSERX9-0jFZHPqIk_XpjNUKDMhK_QFAucef</recordid><startdate>19890801</startdate><enddate>19890801</enddate><creator>OSTER, W</creator><creator>CICCO, N. A</creator><creator>KLEIN, H</creator><creator>HIRANO, T</creator><creator>KISHIMOTO, T</creator><creator>LINDEMANN, A</creator><creator>MERTELSMANN, R. H</creator><creator>HERRMANN, F</creator><general>American Society for Clinical Investigation</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>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19890801</creationdate><title>Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control</title><author>OSTER, W ; CICCO, N. A ; KLEIN, H ; HIRANO, T ; KISHIMOTO, T ; LINDEMANN, A ; MERTELSMANN, R. H ; HERRMANN, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-c20bb179d316f10223fb6de87d1af8d9a687ad122deba3b1aafddcaf7636bc083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Biological and medical sciences</topic><topic>Colony-Stimulating Factors - biosynthesis</topic><topic>Colony-Stimulating Factors - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Interleukin-1 - genetics</topic><topic>Interleukin-1 - physiology</topic><topic>Interleukin-6</topic><topic>Interleukins - genetics</topic><topic>Interleukins - physiology</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OSTER, W</creatorcontrib><creatorcontrib>CICCO, N. A</creatorcontrib><creatorcontrib>KLEIN, H</creatorcontrib><creatorcontrib>HIRANO, T</creatorcontrib><creatorcontrib>KISHIMOTO, T</creatorcontrib><creatorcontrib>LINDEMANN, A</creatorcontrib><creatorcontrib>MERTELSMANN, R. H</creatorcontrib><creatorcontrib>HERRMANN, F</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OSTER, W</au><au>CICCO, N. A</au><au>KLEIN, H</au><au>HIRANO, T</au><au>KISHIMOTO, T</au><au>LINDEMANN, A</au><au>MERTELSMANN, R. H</au><au>HERRMANN, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>1989-08-01</date><risdate>1989</risdate><volume>84</volume><issue>2</issue><spage>451</spage><epage>457</epage><pages>451-457</pages><issn>0021-9738</issn><eissn>1558-8238</eissn><coden>JCINAO</coden><abstract>Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6, TNF-alpha, and IL-1 in growth control of AML were investigated in vitro. We show that a substantial proportion of AML cells produce IL-6, TNF-alpha, and IL-1-beta and use these mediators to stimulate their growth by disparate mechanisms: IL-6 acts as a costimulator to enhance CSF-induced clonogenicity of AML blasts. TNF-alpha induces CSF production by endothelial cells and may therefore provide a paracrine loop to support leukemia growth.</abstract><cop>Ann Arbor, MI</cop><pub>American Society for Clinical Investigation</pub><pmid>2788173</pmid><doi>10.1172/jci114186</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9738 |
| ispartof | The Journal of clinical investigation, 1989-08, Vol.84 (2), p.451-457 |
| issn | 0021-9738 1558-8238 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_548903 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Biological and medical sciences Colony-Stimulating Factors - biosynthesis Colony-Stimulating Factors - genetics Hematologic and hematopoietic diseases Humans Interleukin-1 - genetics Interleukin-1 - physiology Interleukin-6 Interleukins - genetics Interleukins - physiology Leukemia, Myeloid, Acute - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Neoplastic Stem Cells - pathology Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - physiology |
| title | Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T06%3A45%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Participation%20of%20the%20cytokines%20interleukin%206,%20tumor%20necrosis%20factor-alpha,%20and%20interleukin%201-beta%20secreted%20by%20acute%20myelogenous%20leukemia%20blasts%20in%20autocrine%20and%20paracrine%20leukemia%20growth%20control&rft.jtitle=The%20Journal%20of%20clinical%20investigation&rft.au=OSTER,%20W&rft.date=1989-08-01&rft.volume=84&rft.issue=2&rft.spage=451&rft.epage=457&rft.pages=451-457&rft.issn=0021-9738&rft.eissn=1558-8238&rft.coden=JCINAO&rft_id=info:doi/10.1172/jci114186&rft_dat=%3Cproquest_pubme%3E79136466%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=15291064&rft_id=info:pmid/2788173&rfr_iscdi=true |