<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE133516" accession="SRP212620">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP212620</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA551672</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE133516</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>KAT7 maintains myeloid leukemogenesis recruits BRD4 to the promoters of target loci to maintain then MLL-AF9 transcriptional programme</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>Here we investigate the essentiality of lysine acetyltransferase KAT7 in AMLs driven by the MLL-X fusions. We find that KAT7 activity is required for the recruitment of the MLL-fusion associated adaptor proteins such as BRD4 to gene promoters, which are critical for the maintenance of the MLL-AF9 transcriptional programme. Our findings propose that KAT7 is a plausible therapeutic target for this poor prognosis subtype of AML. Overall design: Study KAT7 binding and the effects of its knockout on the transcriptome in MOLM13 and OCIAML3 cell lines</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE133516</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>32764680</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
