Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression
AML with chromosomal alterations involving 3q26 overexpresses the transcription factor (TF) EVI1, associated with therapy refractoriness and inferior overall survival in AML. Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc...
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| Veröffentlicht in: | Leukemia 2024-03, Vol.38 (3), p.545-556 |
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| creator | Birdwell, Christine E. Fiskus, Warren Kadia, Tapan M. Mill, Christopher P. Sasaki, Koji Daver, Naval DiNardo, Courtney D. Pemmaraju, Naveen Borthakur, Gautam Davis, John A. Das, Kaberi Sharma, Sunil Horrigan, Stephen Ruan, Xinjia Su, Xiaoping Khoury, Joseph D. Kantarjian, Hagop Bhalla, Kapil N. |
| description | AML with chromosomal alterations involving 3q26 overexpresses the transcription factor (TF) EVI1, associated with therapy refractoriness and inferior overall survival in AML. Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc, c-Myb, CDK4/6, and MCL1, and induced apoptosis of AML cells with 3q26 lesions. Tegavivint (TV, BC-2059), known to disrupt the binding of nuclear β-catenin and TCF7L2/LEF1 with TBL1, also inhibited co-localization of EVI1 with TBL1 and dose-dependently induced apoptosis in AML cell lines and patient-derived (PD) AML cells with 3q26.2 lesions. TV treatment repressed EVI1, attenuated enhancer activity at ERG, TCF7L2, GATA2 and MECOM loci, abolished interactions between MYC enhancers, repressing AML stemness while upregulating mRNA gene-sets of interferon/inflammatory response, TGF-β signaling and apoptosis-regulation. Co-treatment with TV and BETi or venetoclax induced synergistic in vitro lethality and reduced AML burden, improving survival of NSG mice harboring xenografts of AML with 3q26.2 lesions. |
| doi_str_mv | 10.1038/s41375-023-02108-3 |
| format | Article |
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Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc, c-Myb, CDK4/6, and MCL1, and induced apoptosis of AML cells with 3q26 lesions. Tegavivint (TV, BC-2059), known to disrupt the binding of nuclear β-catenin and TCF7L2/LEF1 with TBL1, also inhibited co-localization of EVI1 with TBL1 and dose-dependently induced apoptosis in AML cell lines and patient-derived (PD) AML cells with 3q26.2 lesions. TV treatment repressed EVI1, attenuated enhancer activity at ERG, TCF7L2, GATA2 and MECOM loci, abolished interactions between MYC enhancers, repressing AML stemness while upregulating mRNA gene-sets of interferon/inflammatory response, TGF-β signaling and apoptosis-regulation. Co-treatment with TV and BETi or venetoclax induced synergistic in vitro lethality and reduced AML burden, improving survival of NSG mice harboring xenografts of AML with 3q26.2 lesions.</description><identifier>ISSN: 0887-6924</identifier><identifier>ISSN: 1476-5551</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/s41375-023-02108-3</identifier><identifier>PMID: 38086946</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14 ; 14/19 ; 14/5 ; 14/63 ; 38 ; 38/109 ; 38/91 ; 631/67/1059/602 ; 631/67/1990/283/1897 ; Apoptosis ; c-Myb protein ; c-Myc protein ; Cancer Research ; Cell lines ; CRISPR ; Critical Care Medicine ; Enhancers ; Epigenetics ; Hematology ; Inflammation ; Inflammatory response ; Intensive ; Internal Medicine ; Lesions ; Lethality ; Localization ; Mcl-1 protein ; Medicine ; Medicine & Public Health ; Myc protein ; Oncology ; Survival ; Thermal resistance ; Transforming growth factor-b ; Xenotransplantation ; β-Catenin</subject><ispartof>Leukemia, 2024-03, Vol.38 (3), p.545-556</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2023. 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The Author(s), under exclusive licence to Springer Nature Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-1f6c7217dd8f78929a3d4d432714d9dcd8f381eb4d0f764722f0676e2af2207e3</cites><orcidid>0000-0003-0957-6009 ; 0000-0001-7679-6453 ; 0000-0001-5209-5126 ; 0000-0001-9003-0390 ; 0000-0002-9892-9832 ; 0000-0002-1670-6513 ; 0000-0003-4702-0386 ; 0000-0002-9140-0610 ; 0000-0001-7103-373X ; 0000-0003-2621-3584 ; 0000-0002-7343-6214</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41375-023-02108-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41375-023-02108-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38086946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Birdwell, Christine E.</creatorcontrib><creatorcontrib>Fiskus, Warren</creatorcontrib><creatorcontrib>Kadia, Tapan M.</creatorcontrib><creatorcontrib>Mill, Christopher P.</creatorcontrib><creatorcontrib>Sasaki, Koji</creatorcontrib><creatorcontrib>Daver, Naval</creatorcontrib><creatorcontrib>DiNardo, Courtney D.</creatorcontrib><creatorcontrib>Pemmaraju, Naveen</creatorcontrib><creatorcontrib>Borthakur, Gautam</creatorcontrib><creatorcontrib>Davis, John A.</creatorcontrib><creatorcontrib>Das, Kaberi</creatorcontrib><creatorcontrib>Sharma, Sunil</creatorcontrib><creatorcontrib>Horrigan, Stephen</creatorcontrib><creatorcontrib>Ruan, Xinjia</creatorcontrib><creatorcontrib>Su, Xiaoping</creatorcontrib><creatorcontrib>Khoury, Joseph D.</creatorcontrib><creatorcontrib>Kantarjian, Hagop</creatorcontrib><creatorcontrib>Bhalla, Kapil N.</creatorcontrib><title>Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>AML with chromosomal alterations involving 3q26 overexpresses the transcription factor (TF) EVI1, associated with therapy refractoriness and inferior overall survival in AML. Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc, c-Myb, CDK4/6, and MCL1, and induced apoptosis of AML cells with 3q26 lesions. Tegavivint (TV, BC-2059), known to disrupt the binding of nuclear β-catenin and TCF7L2/LEF1 with TBL1, also inhibited co-localization of EVI1 with TBL1 and dose-dependently induced apoptosis in AML cell lines and patient-derived (PD) AML cells with 3q26.2 lesions. TV treatment repressed EVI1, attenuated enhancer activity at ERG, TCF7L2, GATA2 and MECOM loci, abolished interactions between MYC enhancers, repressing AML stemness while upregulating mRNA gene-sets of interferon/inflammatory response, TGF-β signaling and apoptosis-regulation. Co-treatment with TV and BETi or venetoclax induced synergistic in vitro lethality and reduced AML burden, improving survival of NSG mice harboring xenografts of AML with 3q26.2 lesions.</description><subject>14</subject><subject>14/19</subject><subject>14/5</subject><subject>14/63</subject><subject>38</subject><subject>38/109</subject><subject>38/91</subject><subject>631/67/1059/602</subject><subject>631/67/1990/283/1897</subject><subject>Apoptosis</subject><subject>c-Myb protein</subject><subject>c-Myc protein</subject><subject>Cancer Research</subject><subject>Cell lines</subject><subject>CRISPR</subject><subject>Critical Care Medicine</subject><subject>Enhancers</subject><subject>Epigenetics</subject><subject>Hematology</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Lesions</subject><subject>Lethality</subject><subject>Localization</subject><subject>Mcl-1 protein</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myc protein</subject><subject>Oncology</subject><subject>Survival</subject><subject>Thermal resistance</subject><subject>Transforming growth factor-b</subject><subject>Xenotransplantation</subject><subject>β-Catenin</subject><issn>0887-6924</issn><issn>1476-5551</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kU9PGzEQxa2qqATaL9BDZakXLgv-t7b3iFAKSKngAL1axh4nRrveYG-gfHscAq3UQw_WWH6_eR7NQ-grJceUcH1SBOWqbQjj9VCiG_4BzahQsmnbln5EM6K1amTHxD46KOWekK0oP6F9romWnZAztLrO4PqYorM9hhBqdc94DHiyeQlTTEsM67iEVO8OD-BWNsUyFBwTPv25wE9xWmH-wCTuocQxFWyTx_NflxSPj5Dh9zpD2Qqf0V6wfYEvb_UQ3f6Y35xdNIur88uz00XjOJNTQ4N0ilHlvQ5Kd6yz3AsvOFNU-M67-sw1hTvhSVBSKMYCkUoCs4ExooAfoqOd7zqPDxsokxlicdD3NsG4KYZ1hHVtJ4Sq6Pd_0Ptxk1OdrlJc0VZTxSrFdpTLYykZglnnONj8bCgx2xzMLgdTczCvORhem769WW_uBvB_Wt4XXwG-A0qV0hLy37__Y_sCl3iSEQ</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Birdwell, Christine E.</creator><creator>Fiskus, Warren</creator><creator>Kadia, Tapan M.</creator><creator>Mill, Christopher P.</creator><creator>Sasaki, Koji</creator><creator>Daver, Naval</creator><creator>DiNardo, Courtney D.</creator><creator>Pemmaraju, Naveen</creator><creator>Borthakur, Gautam</creator><creator>Davis, John A.</creator><creator>Das, Kaberi</creator><creator>Sharma, Sunil</creator><creator>Horrigan, Stephen</creator><creator>Ruan, Xinjia</creator><creator>Su, Xiaoping</creator><creator>Khoury, Joseph D.</creator><creator>Kantarjian, Hagop</creator><creator>Bhalla, Kapil N.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0957-6009</orcidid><orcidid>https://orcid.org/0000-0001-7679-6453</orcidid><orcidid>https://orcid.org/0000-0001-5209-5126</orcidid><orcidid>https://orcid.org/0000-0001-9003-0390</orcidid><orcidid>https://orcid.org/0000-0002-9892-9832</orcidid><orcidid>https://orcid.org/0000-0002-1670-6513</orcidid><orcidid>https://orcid.org/0000-0003-4702-0386</orcidid><orcidid>https://orcid.org/0000-0002-9140-0610</orcidid><orcidid>https://orcid.org/0000-0001-7103-373X</orcidid><orcidid>https://orcid.org/0000-0003-2621-3584</orcidid><orcidid>https://orcid.org/0000-0002-7343-6214</orcidid></search><sort><creationdate>20240301</creationdate><title>Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression</title><author>Birdwell, Christine E. ; 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Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc, c-Myb, CDK4/6, and MCL1, and induced apoptosis of AML cells with 3q26 lesions. Tegavivint (TV, BC-2059), known to disrupt the binding of nuclear β-catenin and TCF7L2/LEF1 with TBL1, also inhibited co-localization of EVI1 with TBL1 and dose-dependently induced apoptosis in AML cell lines and patient-derived (PD) AML cells with 3q26.2 lesions. TV treatment repressed EVI1, attenuated enhancer activity at ERG, TCF7L2, GATA2 and MECOM loci, abolished interactions between MYC enhancers, repressing AML stemness while upregulating mRNA gene-sets of interferon/inflammatory response, TGF-β signaling and apoptosis-regulation. 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| ispartof | Leukemia, 2024-03, Vol.38 (3), p.545-556 |
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| subjects | 14 14/19 14/5 14/63 38 38/109 38/91 631/67/1059/602 631/67/1990/283/1897 Apoptosis c-Myb protein c-Myc protein Cancer Research Cell lines CRISPR Critical Care Medicine Enhancers Epigenetics Hematology Inflammation Inflammatory response Intensive Internal Medicine Lesions Lethality Localization Mcl-1 protein Medicine Medicine & Public Health Myc protein Oncology Survival Thermal resistance Transforming growth factor-b Xenotransplantation β-Catenin |
| title | Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression |
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