Selective JAK2 Inhibition Specifically Decreases Hodgkin Lymphoma and Mediastinal Large B-cell Lymphoma Growth In Vitro and In Vivo
Classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (MLBCL) share similar histologic, clinical, and genetic features. In recent studies, we found that disease-specific chromosome 9p24.1/JAK2 amplification increased JAK2 expression and activity in both cHL and MLBCL. This p...
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| Veröffentlicht in: | Clinical cancer research 2014-05, Vol.20 (10), p.2674-2683 |
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| creator | YANSHENG HAO BJOERN CHAPUY MONTI, Stefano SUN, Heather H RODIG, Scott J SHIPP, Margaret A |
| description | Classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (MLBCL) share similar histologic, clinical, and genetic features. In recent studies, we found that disease-specific chromosome 9p24.1/JAK2 amplification increased JAK2 expression and activity in both cHL and MLBCL. This prompted us to assess the activity of a clinical grade JAK2 selective inhibitor, fedratinib (SAR302503/TG101348), in in vitro and in vivo model systems of cHL and MLBCL with defined JAK2 copy numbers.
We used functional and immunohistochemical analyses to investigate the preclinical activity of fedratinib and associated biomarkers in cell lines and murine xenograft models of cHL and MLBCL with known 9p24.1/JAK2 copy number.
Chemical JAK2 inhibition decreased the cellular proliferation of cHL and MLBCL cell lines and induced their apoptosis. There was an inverse correlation between 9p24.1/JAK2 copy number and the EC50 of fedratinib. Chemical JAK2 inhibition decreased phosphorylation of JAK2, STAT1, STAT3, and STAT6 and reduced the expression of additional downstream targets, including PD-L1, in a copy number-dependent manner. In murine xenograft models of cHL and MLBCL with 9p24.1/JAK2 amplification, chemical JAK2 inhibition significantly decreased JAK2/STAT signaling and tumor growth and prolonged survival. In in vitro and in vivo studies, pSTAT3 was an excellent biomarker of baseline JAK2 activity and the efficacy of chemical JAK2 inhibition.
In in vitro and in vivo analyses, cHL and MLBCL with 9p24.1/JAK2 copy gain are sensitive to chemical JAK2 inhibition suggesting that clinical evaluation of JAK2 blockade is warranted. |
| doi_str_mv | 10.1158/1078-0432.ccr-13-3007 |
| format | Article |
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We used functional and immunohistochemical analyses to investigate the preclinical activity of fedratinib and associated biomarkers in cell lines and murine xenograft models of cHL and MLBCL with known 9p24.1/JAK2 copy number.
Chemical JAK2 inhibition decreased the cellular proliferation of cHL and MLBCL cell lines and induced their apoptosis. There was an inverse correlation between 9p24.1/JAK2 copy number and the EC50 of fedratinib. Chemical JAK2 inhibition decreased phosphorylation of JAK2, STAT1, STAT3, and STAT6 and reduced the expression of additional downstream targets, including PD-L1, in a copy number-dependent manner. In murine xenograft models of cHL and MLBCL with 9p24.1/JAK2 amplification, chemical JAK2 inhibition significantly decreased JAK2/STAT signaling and tumor growth and prolonged survival. In in vitro and in vivo studies, pSTAT3 was an excellent biomarker of baseline JAK2 activity and the efficacy of chemical JAK2 inhibition.
In in vitro and in vivo analyses, cHL and MLBCL with 9p24.1/JAK2 copy gain are sensitive to chemical JAK2 inhibition suggesting that clinical evaluation of JAK2 blockade is warranted.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.ccr-13-3007</identifier><identifier>PMID: 24610827</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Apoptosis - drug effects ; Apoptosis - genetics ; B7-H1 Antigen - genetics ; B7-H1 Antigen - metabolism ; Biological and medical sciences ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Gene Dosage - drug effects ; Gene Expression - drug effects ; Hematologic and hematopoietic diseases ; Hodgkin Disease - genetics ; Hodgkin Disease - metabolism ; Hodgkin Disease - prevention & control ; Humans ; Immunohistochemistry ; Interleukin Receptor Common gamma Subunit - deficiency ; Interleukin Receptor Common gamma Subunit - genetics ; Janus Kinase 2 - antagonists & inhibitors ; Janus Kinase 2 - genetics ; Janus Kinase 2 - metabolism ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoma, Large B-Cell, Diffuse - genetics ; Lymphoma, Large B-Cell, Diffuse - metabolism ; Lymphoma, Large B-Cell, Diffuse - prevention & control ; Male ; Mediastinal Neoplasms - genetics ; Mediastinal Neoplasms - metabolism ; Mediastinal Neoplasms - prevention & control ; Medical sciences ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Pharmacology. Drug treatments ; Pyrrolidines - pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction - drug effects ; STAT Transcription Factors - metabolism ; Sulfonamides - pharmacology ; Tumor Burden - drug effects ; Xenograft Model Antitumor Assays</subject><ispartof>Clinical cancer research, 2014-05, Vol.20 (10), p.2674-2683</ispartof><rights>2015 INIST-CNRS</rights><rights>2014 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-b2136968baf6afe9178e55571dd0f4f442d2bbc186523125f92063529519399a3</citedby><cites>FETCH-LOGICAL-c507t-b2136968baf6afe9178e55571dd0f4f442d2bbc186523125f92063529519399a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3354,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28509652$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24610827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YANSHENG HAO</creatorcontrib><creatorcontrib>BJOERN CHAPUY</creatorcontrib><creatorcontrib>MONTI, Stefano</creatorcontrib><creatorcontrib>SUN, Heather H</creatorcontrib><creatorcontrib>RODIG, Scott J</creatorcontrib><creatorcontrib>SHIPP, Margaret A</creatorcontrib><title>Selective JAK2 Inhibition Specifically Decreases Hodgkin Lymphoma and Mediastinal Large B-cell Lymphoma Growth In Vitro and In Vivo</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (MLBCL) share similar histologic, clinical, and genetic features. In recent studies, we found that disease-specific chromosome 9p24.1/JAK2 amplification increased JAK2 expression and activity in both cHL and MLBCL. This prompted us to assess the activity of a clinical grade JAK2 selective inhibitor, fedratinib (SAR302503/TG101348), in in vitro and in vivo model systems of cHL and MLBCL with defined JAK2 copy numbers.
We used functional and immunohistochemical analyses to investigate the preclinical activity of fedratinib and associated biomarkers in cell lines and murine xenograft models of cHL and MLBCL with known 9p24.1/JAK2 copy number.
Chemical JAK2 inhibition decreased the cellular proliferation of cHL and MLBCL cell lines and induced their apoptosis. There was an inverse correlation between 9p24.1/JAK2 copy number and the EC50 of fedratinib. Chemical JAK2 inhibition decreased phosphorylation of JAK2, STAT1, STAT3, and STAT6 and reduced the expression of additional downstream targets, including PD-L1, in a copy number-dependent manner. In murine xenograft models of cHL and MLBCL with 9p24.1/JAK2 amplification, chemical JAK2 inhibition significantly decreased JAK2/STAT signaling and tumor growth and prolonged survival. In in vitro and in vivo studies, pSTAT3 was an excellent biomarker of baseline JAK2 activity and the efficacy of chemical JAK2 inhibition.
In in vitro and in vivo analyses, cHL and MLBCL with 9p24.1/JAK2 copy gain are sensitive to chemical JAK2 inhibition suggesting that clinical evaluation of JAK2 blockade is warranted.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>B7-H1 Antigen - genetics</subject><subject>B7-H1 Antigen - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Gene Dosage - drug effects</subject><subject>Gene Expression - drug effects</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hodgkin Disease - genetics</subject><subject>Hodgkin Disease - metabolism</subject><subject>Hodgkin Disease - prevention & control</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interleukin Receptor Common gamma Subunit - deficiency</subject><subject>Interleukin Receptor Common gamma Subunit - genetics</subject><subject>Janus Kinase 2 - antagonists & inhibitors</subject><subject>Janus Kinase 2 - genetics</subject><subject>Janus Kinase 2 - metabolism</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoma, Large B-Cell, Diffuse - genetics</subject><subject>Lymphoma, Large B-Cell, Diffuse - metabolism</subject><subject>Lymphoma, Large B-Cell, Diffuse - prevention & control</subject><subject>Male</subject><subject>Mediastinal Neoplasms - genetics</subject><subject>Mediastinal Neoplasms - metabolism</subject><subject>Mediastinal Neoplasms - prevention & control</subject><subject>Medical sciences</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Knockout</subject><subject>Mice, SCID</subject><subject>Pharmacology. Drug treatments</subject><subject>Pyrrolidines - pharmacology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal Transduction - drug effects</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Sulfonamides - pharmacology</subject><subject>Tumor Burden - drug effects</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUlPwzAUhC0EYin8BJAvHAN-XrJckKDsFCGxXS3HsVtDGld2KOqZP07Czsm2_M08vRmEtoHsAYh8H0iWJ4Qzuqd1SIAljJBsCa2DEFnCaCqWu_s3s4Y2YnwiBDgQvorWKE-B5DRbR293pja6dXODLw-vKL5oJq50rfMNvpsZ7azTqq4X-NjoYFQ0EZ_7avzsGjxaTGcTP1VYNRW-NpVTsXWNqvFIhbHBR4k2df1LnQX_2k46f_zo2uA_VB-Pud9EK1bV0Wx9nQP0cHpyPzxPRjdnF8PDUaIFydqkpMDSIs1LZVNlTQFZbkS3LVQVsdxyTitalhryVFAGVNiCkpQJWggoWFEoNkAHn76zl3JqKm2aNqhazoKbqrCQXjn5_6dxEzn2c8lJzrMuxwESnwY6-BiDsT9aILJvRfaJyz5xORzeSmCyb6XT7fwd_KP6rqEDdr8AFbu8bVCNdvGXywUp-q3eAaxqlrE</recordid><startdate>20140515</startdate><enddate>20140515</enddate><creator>YANSHENG HAO</creator><creator>BJOERN CHAPUY</creator><creator>MONTI, Stefano</creator><creator>SUN, Heather H</creator><creator>RODIG, Scott J</creator><creator>SHIPP, Margaret A</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>5PM</scope></search><sort><creationdate>20140515</creationdate><title>Selective JAK2 Inhibition Specifically Decreases Hodgkin Lymphoma and Mediastinal Large B-cell Lymphoma Growth In Vitro and In Vivo</title><author>YANSHENG HAO ; BJOERN CHAPUY ; MONTI, Stefano ; SUN, Heather H ; RODIG, Scott J ; SHIPP, Margaret A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-b2136968baf6afe9178e55571dd0f4f442d2bbc186523125f92063529519399a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>B7-H1 Antigen - genetics</topic><topic>B7-H1 Antigen - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Gene Dosage - drug effects</topic><topic>Gene Expression - drug effects</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hodgkin Disease - genetics</topic><topic>Hodgkin Disease - metabolism</topic><topic>Hodgkin Disease - prevention & control</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Interleukin Receptor Common gamma Subunit - deficiency</topic><topic>Interleukin Receptor Common gamma Subunit - genetics</topic><topic>Janus Kinase 2 - antagonists & inhibitors</topic><topic>Janus Kinase 2 - genetics</topic><topic>Janus Kinase 2 - metabolism</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphoma, Large B-Cell, Diffuse - genetics</topic><topic>Lymphoma, Large B-Cell, Diffuse - metabolism</topic><topic>Lymphoma, Large B-Cell, Diffuse - prevention & control</topic><topic>Male</topic><topic>Mediastinal Neoplasms - genetics</topic><topic>Mediastinal Neoplasms - metabolism</topic><topic>Mediastinal Neoplasms - prevention & control</topic><topic>Medical sciences</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Knockout</topic><topic>Mice, SCID</topic><topic>Pharmacology. Drug treatments</topic><topic>Pyrrolidines - pharmacology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Signal Transduction - drug effects</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Sulfonamides - pharmacology</topic><topic>Tumor Burden - drug effects</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YANSHENG HAO</creatorcontrib><creatorcontrib>BJOERN CHAPUY</creatorcontrib><creatorcontrib>MONTI, Stefano</creatorcontrib><creatorcontrib>SUN, Heather H</creatorcontrib><creatorcontrib>RODIG, Scott J</creatorcontrib><creatorcontrib>SHIPP, Margaret A</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>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YANSHENG HAO</au><au>BJOERN CHAPUY</au><au>MONTI, Stefano</au><au>SUN, Heather H</au><au>RODIG, Scott J</au><au>SHIPP, Margaret A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective JAK2 Inhibition Specifically Decreases Hodgkin Lymphoma and Mediastinal Large B-cell Lymphoma Growth In Vitro and In Vivo</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2014-05-15</date><risdate>2014</risdate><volume>20</volume><issue>10</issue><spage>2674</spage><epage>2683</epage><pages>2674-2683</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (MLBCL) share similar histologic, clinical, and genetic features. In recent studies, we found that disease-specific chromosome 9p24.1/JAK2 amplification increased JAK2 expression and activity in both cHL and MLBCL. This prompted us to assess the activity of a clinical grade JAK2 selective inhibitor, fedratinib (SAR302503/TG101348), in in vitro and in vivo model systems of cHL and MLBCL with defined JAK2 copy numbers.
We used functional and immunohistochemical analyses to investigate the preclinical activity of fedratinib and associated biomarkers in cell lines and murine xenograft models of cHL and MLBCL with known 9p24.1/JAK2 copy number.
Chemical JAK2 inhibition decreased the cellular proliferation of cHL and MLBCL cell lines and induced their apoptosis. There was an inverse correlation between 9p24.1/JAK2 copy number and the EC50 of fedratinib. Chemical JAK2 inhibition decreased phosphorylation of JAK2, STAT1, STAT3, and STAT6 and reduced the expression of additional downstream targets, including PD-L1, in a copy number-dependent manner. In murine xenograft models of cHL and MLBCL with 9p24.1/JAK2 amplification, chemical JAK2 inhibition significantly decreased JAK2/STAT signaling and tumor growth and prolonged survival. In in vitro and in vivo studies, pSTAT3 was an excellent biomarker of baseline JAK2 activity and the efficacy of chemical JAK2 inhibition.
In in vitro and in vivo analyses, cHL and MLBCL with 9p24.1/JAK2 copy gain are sensitive to chemical JAK2 inhibition suggesting that clinical evaluation of JAK2 blockade is warranted.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>24610827</pmid><doi>10.1158/1078-0432.ccr-13-3007</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic agents Apoptosis - drug effects Apoptosis - genetics B7-H1 Antigen - genetics B7-H1 Antigen - metabolism Biological and medical sciences Blotting, Western Cell Line, Tumor Cell Proliferation - drug effects Gene Dosage - drug effects Gene Expression - drug effects Hematologic and hematopoietic diseases Hodgkin Disease - genetics Hodgkin Disease - metabolism Hodgkin Disease - prevention & control Humans Immunohistochemistry Interleukin Receptor Common gamma Subunit - deficiency Interleukin Receptor Common gamma Subunit - genetics Janus Kinase 2 - antagonists & inhibitors Janus Kinase 2 - genetics Janus Kinase 2 - metabolism Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoma, Large B-Cell, Diffuse - genetics Lymphoma, Large B-Cell, Diffuse - metabolism Lymphoma, Large B-Cell, Diffuse - prevention & control Male Mediastinal Neoplasms - genetics Mediastinal Neoplasms - metabolism Mediastinal Neoplasms - prevention & control Medical sciences Mice, Inbred NOD Mice, Knockout Mice, SCID Pharmacology. Drug treatments Pyrrolidines - pharmacology Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - drug effects STAT Transcription Factors - metabolism Sulfonamides - pharmacology Tumor Burden - drug effects Xenograft Model Antitumor Assays |
| title | Selective JAK2 Inhibition Specifically Decreases Hodgkin Lymphoma and Mediastinal Large B-cell Lymphoma Growth In Vitro and In Vivo |
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