Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos

The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Blood 2005-09, Vol.106 (6), p.2147-2155
Hauptverfasser: Maki, Kazuhiro, Yamagata, Tetsuya, Asai, Takashi, Yamazaki, Ieharu, Oda, Hideaki, Hirai, Hisamaru, Mitani, Kinuko
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 2155
container_issue 6
container_start_page 2147
container_title Blood
container_volume 106
creator Maki, Kazuhiro
Yamagata, Tetsuya
Asai, Takashi
Yamazaki, Ieharu
Oda, Hideaki
Hirai, Hisamaru
Mitani, Kinuko
description The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.5 (E13.5) as a result of hemorrhage in the central nervous system. The peripheral blood had yolk-sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. Although E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitors from E13.5 AML1/EVI1/+ fetal liver were highly capable of self-renewal compared with those from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/EVI1/+ fetal liver. (Blood. 2005;106:2147-2155)
doi_str_mv 10.1182/blood-2004-11-4330
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68551894</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006497120634413</els_id><sourcerecordid>68551894</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4090-9f0c4ea58cd68233201cec4c3968b6184e011cf5b47e2a477345ca0cfa2ea9803</originalsourceid><addsrcrecordid>eNp9kE1v1DAQhi0EotvSP8AB5QI30xl_JI7EZVVaqLSIC_RqOZOJME3iJc5W2n_fbHel3jiNZvS8r0aPEO8RPiM6ddX0KbVSARiJKI3W8Eqs0ConARS8FisAKKWpKzwT5zn_BUCjlX0rztDWaGxpVmL9dZ-3fchzpKLlLo5xjo9c_OEhzGmbIueYizgW6x8bvLq5v8PiYUz0IJcTD820T_mdeNOFPvPlaV6I37c3v66_y83Pb3fX640kAzXIugMyHKyjtnRKawVITIZ0XbqmRGcYEKmzjalYBVNV2lgKQF1QHGoH-kJ8OvZup_Rvx3n2Q8zEfR9GTrvsS2ctutosoDqCNKWcJ-78dopDmPYewR_E-Wdx_iBu2f1B3BL6cGrfNQO3L5GTqQX4eAJCptB3Uxgp5heuQlPp0i3clyPHi4vHyJPPFHkkbuPENPs2xf_98QT-Bon9</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68551894</pqid></control><display><type>article</type><title>Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Maki, Kazuhiro ; Yamagata, Tetsuya ; Asai, Takashi ; Yamazaki, Ieharu ; Oda, Hideaki ; Hirai, Hisamaru ; Mitani, Kinuko</creator><creatorcontrib>Maki, Kazuhiro ; Yamagata, Tetsuya ; Asai, Takashi ; Yamazaki, Ieharu ; Oda, Hideaki ; Hirai, Hisamaru ; Mitani, Kinuko</creatorcontrib><description>The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.5 (E13.5) as a result of hemorrhage in the central nervous system. The peripheral blood had yolk-sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. Although E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitors from E13.5 AML1/EVI1/+ fetal liver were highly capable of self-renewal compared with those from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/EVI1/+ fetal liver. (Blood. 2005;106:2147-2155)</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2004-11-4330</identifier><identifier>PMID: 15914564</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; Animals ; Biological and medical sciences ; Core Binding Factor Alpha 2 Subunit ; DNA-Binding Proteins - genetics ; Embryo, Mammalian ; Erythroblasts ; Hematologic and hematopoietic diseases ; Hematopoiesis - genetics ; Hematopoietic Stem Cells - cytology ; Intracranial Hemorrhages - etiology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; LIM Domain Proteins ; Liver - cytology ; Liver - embryology ; MDS1 and EVI1 Complex Locus Protein ; Medical sciences ; Metalloproteins - genetics ; Mice ; Mice, Transgenic ; Multipotent Stem Cells ; Oncogene Proteins, Fusion - genetics ; Oncogene Proteins, Fusion - physiology ; Proto-Oncogene Proteins - genetics ; Proto-Oncogenes - genetics ; Trans-Activators - genetics ; Transcription Factors - genetics</subject><ispartof>Blood, 2005-09, Vol.106 (6), p.2147-2155</ispartof><rights>2005 American Society of Hematology</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4090-9f0c4ea58cd68233201cec4c3968b6184e011cf5b47e2a477345ca0cfa2ea9803</citedby><cites>FETCH-LOGICAL-c4090-9f0c4ea58cd68233201cec4c3968b6184e011cf5b47e2a477345ca0cfa2ea9803</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=17147368$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15914564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maki, Kazuhiro</creatorcontrib><creatorcontrib>Yamagata, Tetsuya</creatorcontrib><creatorcontrib>Asai, Takashi</creatorcontrib><creatorcontrib>Yamazaki, Ieharu</creatorcontrib><creatorcontrib>Oda, Hideaki</creatorcontrib><creatorcontrib>Hirai, Hisamaru</creatorcontrib><creatorcontrib>Mitani, Kinuko</creatorcontrib><title>Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos</title><title>Blood</title><addtitle>Blood</addtitle><description>The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.5 (E13.5) as a result of hemorrhage in the central nervous system. The peripheral blood had yolk-sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. Although E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitors from E13.5 AML1/EVI1/+ fetal liver were highly capable of self-renewal compared with those from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/EVI1/+ fetal liver. (Blood. 2005;106:2147-2155)</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Core Binding Factor Alpha 2 Subunit</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Embryo, Mammalian</subject><subject>Erythroblasts</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematopoiesis - genetics</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Intracranial Hemorrhages - etiology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>LIM Domain Proteins</subject><subject>Liver - cytology</subject><subject>Liver - embryology</subject><subject>MDS1 and EVI1 Complex Locus Protein</subject><subject>Medical sciences</subject><subject>Metalloproteins - genetics</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Multipotent Stem Cells</subject><subject>Oncogene Proteins, Fusion - genetics</subject><subject>Oncogene Proteins, Fusion - physiology</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogenes - genetics</subject><subject>Trans-Activators - genetics</subject><subject>Transcription Factors - genetics</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EotvSP8AB5QI30xl_JI7EZVVaqLSIC_RqOZOJME3iJc5W2n_fbHel3jiNZvS8r0aPEO8RPiM6ddX0KbVSARiJKI3W8Eqs0ConARS8FisAKKWpKzwT5zn_BUCjlX0rztDWaGxpVmL9dZ-3fchzpKLlLo5xjo9c_OEhzGmbIueYizgW6x8bvLq5v8PiYUz0IJcTD820T_mdeNOFPvPlaV6I37c3v66_y83Pb3fX640kAzXIugMyHKyjtnRKawVITIZ0XbqmRGcYEKmzjalYBVNV2lgKQF1QHGoH-kJ8OvZup_Rvx3n2Q8zEfR9GTrvsS2ctutosoDqCNKWcJ-78dopDmPYewR_E-Wdx_iBu2f1B3BL6cGrfNQO3L5GTqQX4eAJCptB3Uxgp5heuQlPp0i3clyPHi4vHyJPPFHkkbuPENPs2xf_98QT-Bon9</recordid><startdate>20050915</startdate><enddate>20050915</enddate><creator>Maki, Kazuhiro</creator><creator>Yamagata, Tetsuya</creator><creator>Asai, Takashi</creator><creator>Yamazaki, Ieharu</creator><creator>Oda, Hideaki</creator><creator>Hirai, Hisamaru</creator><creator>Mitani, Kinuko</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>20050915</creationdate><title>Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos</title><author>Maki, Kazuhiro ; Yamagata, Tetsuya ; Asai, Takashi ; Yamazaki, Ieharu ; Oda, Hideaki ; Hirai, Hisamaru ; Mitani, Kinuko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4090-9f0c4ea58cd68233201cec4c3968b6184e011cf5b47e2a477345ca0cfa2ea9803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Core Binding Factor Alpha 2 Subunit</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Embryo, Mammalian</topic><topic>Erythroblasts</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematopoiesis - genetics</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>Intracranial Hemorrhages - etiology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>LIM Domain Proteins</topic><topic>Liver - cytology</topic><topic>Liver - embryology</topic><topic>MDS1 and EVI1 Complex Locus Protein</topic><topic>Medical sciences</topic><topic>Metalloproteins - genetics</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Multipotent Stem Cells</topic><topic>Oncogene Proteins, Fusion - genetics</topic><topic>Oncogene Proteins, Fusion - physiology</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogenes - genetics</topic><topic>Trans-Activators - genetics</topic><topic>Transcription Factors - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maki, Kazuhiro</creatorcontrib><creatorcontrib>Yamagata, Tetsuya</creatorcontrib><creatorcontrib>Asai, Takashi</creatorcontrib><creatorcontrib>Yamazaki, Ieharu</creatorcontrib><creatorcontrib>Oda, Hideaki</creatorcontrib><creatorcontrib>Hirai, Hisamaru</creatorcontrib><creatorcontrib>Mitani, Kinuko</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maki, Kazuhiro</au><au>Yamagata, Tetsuya</au><au>Asai, Takashi</au><au>Yamazaki, Ieharu</au><au>Oda, Hideaki</au><au>Hirai, Hisamaru</au><au>Mitani, Kinuko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2005-09-15</date><risdate>2005</risdate><volume>106</volume><issue>6</issue><spage>2147</spage><epage>2155</epage><pages>2147-2155</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.5 (E13.5) as a result of hemorrhage in the central nervous system. The peripheral blood had yolk-sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. Although E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitors from E13.5 AML1/EVI1/+ fetal liver were highly capable of self-renewal compared with those from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/EVI1/+ fetal liver. (Blood. 2005;106:2147-2155)</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>15914564</pmid><doi>10.1182/blood-2004-11-4330</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0006-4971
ispartof Blood, 2005-09, Vol.106 (6), p.2147-2155
issn 0006-4971
1528-0020
language eng
recordid cdi_proquest_miscellaneous_68551894
source MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection
subjects Adaptor Proteins, Signal Transducing
Animals
Biological and medical sciences
Core Binding Factor Alpha 2 Subunit
DNA-Binding Proteins - genetics
Embryo, Mammalian
Erythroblasts
Hematologic and hematopoietic diseases
Hematopoiesis - genetics
Hematopoietic Stem Cells - cytology
Intracranial Hemorrhages - etiology
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
LIM Domain Proteins
Liver - cytology
Liver - embryology
MDS1 and EVI1 Complex Locus Protein
Medical sciences
Metalloproteins - genetics
Mice
Mice, Transgenic
Multipotent Stem Cells
Oncogene Proteins, Fusion - genetics
Oncogene Proteins, Fusion - physiology
Proto-Oncogene Proteins - genetics
Proto-Oncogenes - genetics
Trans-Activators - genetics
Transcription Factors - genetics
title Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T13%3A40%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dysplastic%20definitive%20hematopoiesis%20in%20AML1/EVI1%20knock-in%20embryos&rft.jtitle=Blood&rft.au=Maki,%20Kazuhiro&rft.date=2005-09-15&rft.volume=106&rft.issue=6&rft.spage=2147&rft.epage=2155&rft.pages=2147-2155&rft.issn=0006-4971&rft.eissn=1528-0020&rft_id=info:doi/10.1182/blood-2004-11-4330&rft_dat=%3Cproquest_cross%3E68551894%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=68551894&rft_id=info:pmid/15914564&rft_els_id=S0006497120634413&rfr_iscdi=true