Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis
AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the AML1 gene, at least three isoforms, AML1a , AML1b and AML1c , are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In thi...
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| Veröffentlicht in: | Leukemia 2009-04, Vol.23 (4), p.739-745 |
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| creator | Liu, X Zhang, Q Zhang, D-E Zhou, C Xing, H Tian, Z Rao, Q Wang, M Wang, J |
| description | AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the
AML1
gene, at least three isoforms,
AML1a
,
AML1b
and
AML1c
, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In this study, we found a higher expression level of
AML1a
in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls. Additionally, AML1a represses transcription of promoter of macrophage colony-stimulating factor receptor mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. To investigate the role of
AML1a
in hematopoiesis and leukemogenesis
in vivo
, murine bone marrow mononuclear cells were transduced with
AML1a
and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of
AML1a
may be an important contributing factor to leukemogenesis. |
| doi_str_mv | 10.1038/leu.2008.350 |
| format | Article |
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AML1
gene, at least three isoforms,
AML1a
,
AML1b
and
AML1c
, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In this study, we found a higher expression level of
AML1a
in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls. Additionally, AML1a represses transcription of promoter of macrophage colony-stimulating factor receptor mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. To investigate the role of
AML1a
in hematopoiesis and leukemogenesis
in vivo
, murine bone marrow mononuclear cells were transduced with
AML1a
and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of
AML1a
may be an important contributing factor to leukemogenesis.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/leu.2008.350</identifier><identifier>PMID: 19151769</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acute Disease ; Acute lymphoblastic leukemia ; Acute myeloid leukemia ; Alternative splicing ; AML1 gene ; AML1 protein ; Animals ; Biological and medical sciences ; Bone marrow ; Bone Marrow Cells - metabolism ; Bone Marrow Transplantation ; Cancer Research ; Case-Control Studies ; Cell differentiation ; Colony-stimulating factor ; Core Binding Factor Alpha 2 Subunit - genetics ; Critical Care Medicine ; Differentiation (biology) ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Hematologic and hematopoietic diseases ; Hematology ; Hematopoiesis ; Hospitals ; Humans ; In vivo methods and tests ; Intensive ; Internal Medicine ; Isoforms ; Leukemia ; Leukemia - etiology ; Leukemia - genetics ; Leukemia, Myeloid, Acute - etiology ; Leukemia, Myeloid, Acute - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Leukemogenesis ; Leukocytes (mononuclear) ; Lymphatic leukemia ; Macrophage colony-stimulating factor ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Oncology ; original-article ; Physiological aspects ; Plasmids ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Promoter Regions, Genetic ; Protein Isoforms - genetics ; Receptor, Macrophage Colony-Stimulating Factor - genetics ; Runx1 protein ; Transcription factors ; Transcription, Genetic ; Transduction, Genetic ; Transplantation</subject><ispartof>Leukemia, 2009-04, Vol.23 (4), p.739-745</ispartof><rights>Macmillan Publishers Limited 2009</rights><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 2009</rights><rights>Macmillan Publishers Limited 2009.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c607t-4227fa1ce376b46c24ad4437aea095bc6f35418842cf72b9f5da36bf97fbc00c3</citedby><cites>FETCH-LOGICAL-c607t-4227fa1ce376b46c24ad4437aea095bc6f35418842cf72b9f5da36bf97fbc00c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/leu.2008.350$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/leu.2008.350$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21431640$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19151769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Zhang, Q</creatorcontrib><creatorcontrib>Zhang, D-E</creatorcontrib><creatorcontrib>Zhou, C</creatorcontrib><creatorcontrib>Xing, H</creatorcontrib><creatorcontrib>Tian, Z</creatorcontrib><creatorcontrib>Rao, Q</creatorcontrib><creatorcontrib>Wang, M</creatorcontrib><creatorcontrib>Wang, J</creatorcontrib><title>Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the
AML1
gene, at least three isoforms,
AML1a
,
AML1b
and
AML1c
, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In this study, we found a higher expression level of
AML1a
in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls. Additionally, AML1a represses transcription of promoter of macrophage colony-stimulating factor receptor mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. To investigate the role of
AML1a
in hematopoiesis and leukemogenesis
in vivo
, murine bone marrow mononuclear cells were transduced with
AML1a
and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of
AML1a
may be an important contributing factor to leukemogenesis.</description><subject>Acute Disease</subject><subject>Acute lymphoblastic leukemia</subject><subject>Acute myeloid leukemia</subject><subject>Alternative splicing</subject><subject>AML1 gene</subject><subject>AML1 protein</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Transplantation</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>Cell differentiation</subject><subject>Colony-stimulating factor</subject><subject>Core Binding Factor Alpha 2 Subunit - genetics</subject><subject>Critical Care Medicine</subject><subject>Differentiation (biology)</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Hematopoiesis</subject><subject>Hospitals</subject><subject>Humans</subject><subject>In vivo methods and tests</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Isoforms</subject><subject>Leukemia</subject><subject>Leukemia - etiology</subject><subject>Leukemia - genetics</subject><subject>Leukemia, Myeloid, Acute - etiology</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Leukemogenesis</subject><subject>Leukocytes (mononuclear)</subject><subject>Lymphatic leukemia</subject><subject>Macrophage colony-stimulating factor</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Oncology</subject><subject>original-article</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Isoforms - genetics</subject><subject>Receptor, Macrophage Colony-Stimulating Factor - genetics</subject><subject>Runx1 protein</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Transduction, Genetic</subject><subject>Transplantation</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0s2P1CAYB-DGaNxx9ebZNBr3ZEegfJTjZONXMmYveiaUvsyyUhih3eh_L81MHNesMRwaysP7C_BW1XOM1hi13VsP85og1K1bhh5UK0wFbxhj-GG1Ql0nGi4JPaue5HyD0LLIH1dnWGKGBZerSl3dQoIf-wQ5uxjqaGsdapejjWlcZpvPW1y7UGszT1CXsG8wOl3QULsp1_s4QZic9nWKHhZ4IHEHAbLLT6tHVvsMz47f8-rr-3dfLj8226sPny4328ZwJKaGEiKsxgZawXvKDaF6oLQVGjSSrDfctozirqPEWEF6admgW95bKWxvEDLteXVxqLtP8fsMeVKjywa81wHinBUXmLRdKfk_SBAviZIU-OoveBPnFMohFOGUiZZyKot6-U9FEBOkk-hUaqc9KBdsnJI2S67aYNlRzARaAtf3qDKGcuMmBrCu_L-z4eKPDdeg_XSdo5-n8pD5LnxzgCbFnBNYtU9u1OmnwkgtTaTKo6mliVRposJfHM809yMMJ3zsmgJeH4HORnubdDAu_3YE0xZzuhRqDi6XpbCDdLqce4N_AZT12jo</recordid><startdate>20090401</startdate><enddate>20090401</enddate><creator>Liu, X</creator><creator>Zhang, Q</creator><creator>Zhang, D-E</creator><creator>Zhou, C</creator><creator>Xing, H</creator><creator>Tian, Z</creator><creator>Rao, Q</creator><creator>Wang, M</creator><creator>Wang, J</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7QL</scope><scope>7RV</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20090401</creationdate><title>Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis</title><author>Liu, X ; Zhang, Q ; Zhang, D-E ; Zhou, C ; Xing, H ; Tian, Z ; Rao, Q ; Wang, M ; Wang, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c607t-4227fa1ce376b46c24ad4437aea095bc6f35418842cf72b9f5da36bf97fbc00c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acute Disease</topic><topic>Acute lymphoblastic leukemia</topic><topic>Acute myeloid leukemia</topic><topic>Alternative splicing</topic><topic>AML1 gene</topic><topic>AML1 protein</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone Marrow Transplantation</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Cell differentiation</topic><topic>Colony-stimulating factor</topic><topic>Core Binding Factor Alpha 2 Subunit - genetics</topic><topic>Critical Care Medicine</topic><topic>Differentiation (biology)</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Hematopoiesis</topic><topic>Hospitals</topic><topic>Humans</topic><topic>In vivo methods and tests</topic><topic>Intensive</topic><topic>Internal Medicine</topic><topic>Isoforms</topic><topic>Leukemia</topic><topic>Leukemia - etiology</topic><topic>Leukemia - genetics</topic><topic>Leukemia, Myeloid, Acute - etiology</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Leukemogenesis</topic><topic>Leukocytes (mononuclear)</topic><topic>Lymphatic leukemia</topic><topic>Macrophage colony-stimulating factor</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Oncology</topic><topic>original-article</topic><topic>Physiological aspects</topic><topic>Plasmids</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Isoforms - genetics</topic><topic>Receptor, Macrophage Colony-Stimulating Factor - genetics</topic><topic>Runx1 protein</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Transduction, Genetic</topic><topic>Transplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Zhang, Q</creatorcontrib><creatorcontrib>Zhang, D-E</creatorcontrib><creatorcontrib>Zhou, C</creatorcontrib><creatorcontrib>Xing, H</creatorcontrib><creatorcontrib>Tian, Z</creatorcontrib><creatorcontrib>Rao, Q</creatorcontrib><creatorcontrib>Wang, M</creatorcontrib><creatorcontrib>Wang, J</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 Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Leukemia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, X</au><au>Zhang, Q</au><au>Zhang, D-E</au><au>Zhou, C</au><au>Xing, H</au><au>Tian, Z</au><au>Rao, Q</au><au>Wang, M</au><au>Wang, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis</atitle><jtitle>Leukemia</jtitle><stitle>Leukemia</stitle><addtitle>Leukemia</addtitle><date>2009-04-01</date><risdate>2009</risdate><volume>23</volume><issue>4</issue><spage>739</spage><epage>745</epage><pages>739-745</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><coden>LEUKED</coden><abstract>AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the
AML1
gene, at least three isoforms,
AML1a
,
AML1b
and
AML1c
, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In this study, we found a higher expression level of
AML1a
in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls. Additionally, AML1a represses transcription of promoter of macrophage colony-stimulating factor receptor mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. To investigate the role of
AML1a
in hematopoiesis and leukemogenesis
in vivo
, murine bone marrow mononuclear cells were transduced with
AML1a
and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of
AML1a
may be an important contributing factor to leukemogenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19151769</pmid><doi>10.1038/leu.2008.350</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 0887-6924 |
| ispartof | Leukemia, 2009-04, Vol.23 (4), p.739-745 |
| issn | 0887-6924 1476-5551 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67123844 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature - Complete Springer Journals; Nature Journals Online |
| subjects | Acute Disease Acute lymphoblastic leukemia Acute myeloid leukemia Alternative splicing AML1 gene AML1 protein Animals Biological and medical sciences Bone marrow Bone Marrow Cells - metabolism Bone Marrow Transplantation Cancer Research Case-Control Studies Cell differentiation Colony-stimulating factor Core Binding Factor Alpha 2 Subunit - genetics Critical Care Medicine Differentiation (biology) Gene expression Gene Expression Regulation, Neoplastic Genes Genetic aspects Hematologic and hematopoietic diseases Hematology Hematopoiesis Hospitals Humans In vivo methods and tests Intensive Internal Medicine Isoforms Leukemia Leukemia - etiology Leukemia - genetics Leukemia, Myeloid, Acute - etiology Leukemia, Myeloid, Acute - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Leukemogenesis Leukocytes (mononuclear) Lymphatic leukemia Macrophage colony-stimulating factor Medical sciences Medicine Medicine & Public Health Mice Oncology original-article Physiological aspects Plasmids Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Promoter Regions, Genetic Protein Isoforms - genetics Receptor, Macrophage Colony-Stimulating Factor - genetics Runx1 protein Transcription factors Transcription, Genetic Transduction, Genetic Transplantation |
| title | Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis |
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