<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>103(2)</volume><submitter>Schneider E</submitter><funding>CIHR</funding><pubmed_abstract>Micro-ribonucleic acid-155 (miR-155) is one of the first described oncogenic miRNAs. Although multiple direct targets of miR-155 have been identified, it is not clear how it contributes to the pathogenesis of acute myeloid leukemia. We found miR-155 to be a direct target of Meis1 in murine Hoxa9/Meis1 induced acute myeloid leukemia. The additional overexpression of miR-155 accelerated the formation of acute myeloid leukemia in Hoxa9 as well as in Hoxa9/Meis1 cells &lt;i>in vivo&lt;/i> However, in the absence or following the removal of miR-155, leukemia onset and progression were unaffected. Although miR-155 accelerated growth and homing in addition to impairing differentiation, our data underscore the pathophysiological relevance of miR-155 as an accelerator rather than a driver of leukemogenes</pubmed_abstract><journal>Haematologica</journal><pagination>246-255</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5792269</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Micro-ribonucleic acid-155 is a direct target of Meis1, but not a driver in acute myeloid leukemia.</pubmed_title><pmcid>PMC5792269</pmcid><pubmed_authors>Heuser M</pubmed_authors><pubmed_authors>Xiang P</pubmed_authors><pubmed_authors>Bullinger L</pubmed_authors><pubmed_authors>Ashouri A</pubmed_authors><pubmed_authors>Arabanian L</pubmed_authors><pubmed_authors>Dohner K</pubmed_authors><pubmed_authors>Rouhi A</pubmed_authors><pubmed_authors>Schneider E</pubmed_authors><pubmed_authors>Rohner L</pubmed_authors><pubmed_authors>Buske C</pubmed_authors><pubmed_authors>Hirst M</pubmed_authors><pubmed_authors>Miller C</pubmed_authors><pubmed_authors>Pochert N</pubmed_authors><pubmed_authors>Palmqvist L</pubmed_authors><pubmed_authors>Staffas A</pubmed_authors><pubmed_authors>Wei SY</pubmed_authors><pubmed_authors>Dohner H</pubmed_authors><pubmed_authors>Hansen CL</pubmed_authors><pubmed_authors>Humphries RK</pubmed_authors><pubmed_authors>Ruschmann J</pubmed_authors><pubmed_authors>Petriv OI</pubmed_authors><pubmed_authors>Krowiorz K</pubmed_authors><pubmed_authors>Fogelstrand L</pubmed_authors><pubmed_authors>Kuchenbauer F</pubmed_authors><pubmed_authors>Heravi-Moussavi A</pubmed_authors><pubmed_authors>Malmberg ED</pubmed_authors></additional><is_claimable>false</is_claimable><name>Micro-ribonucleic acid-155 is a direct target of Meis1, but not a driver in acute myeloid leukemia.</name><description>Micro-ribonucleic acid-155 (miR-155) is one of the first described oncogenic miRNAs. Although multiple direct targets of miR-155 have been identified, it is not clear how it contributes to the pathogenesis of acute myeloid leukemia. We found miR-155 to be a direct target of Meis1 in murine Hoxa9/Meis1 induced acute myeloid leukemia. The additional overexpression of miR-155 accelerated the formation of acute myeloid leukemia in Hoxa9 as well as in Hoxa9/Meis1 cells &lt;i>in vivo&lt;/i> However, in the absence or following the removal of miR-155, leukemia onset and progression were unaffected. Although miR-155 accelerated growth and homing in addition to impairing differentiation, our data underscore the pathophysiological relevance of miR-155 as an accelerator rather than a driver of leukemogenes</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Feb</publication><modification>2026-04-15T21:15:17.928Z</modification><creation>2019-06-06T18:51:59Z</creation></dates><accession>S-EPMC5792269</accession><cross_references><pubmed>29217774</pubmed><doi>10.3324/haematol.2017.177485</doi></cross_references></HashMap>