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  <contributors>
    <authors>
      <author>Romine, Kyle</author>
    </authors>
    <secondary-authors>
      <author>Tyner, Jeffrey</author>
    </secondary-authors>
  </contributors>
  <titles>
    <title>Targeting epigenetic dysregulation in acute myeloid leukemia via BET protein inhibition: mechanisms of resistance and contributions towards the anti-tumor response</title>
    <translated-title/>
    <tertiary-title/>
  </titles>
  <periodical>
    <full-title/>
  </periodical>
  <alt-periodical>
    <full-title/>
    <abbr-1/>
  </alt-periodical>
  <pages/>
  <section/>
  <volume/>
  <number/>
  <keywords>
    <keyword>epigenetics</keyword>
    <keyword>brd4</keyword>
    <keyword>Standard of Care</keyword>
    <keyword>T-Lymphocytes</keyword>
    <keyword>T-Cell Exhaustion</keyword>
    <keyword>Leukemia, Myeloid, Acute</keyword>
  </keywords>
  <dates>
    <year>2022</year>
    <pub-dates>
      <date>2022</date>
    </pub-dates>
  </dates>
  <abstract>Acute Myeloid Leukemia (AML) is a genetically and phenotypically heterogeneous white blood cell cancer with a poor prognosis and limited therapeutic options. For many decades the current standard of care has been an intensive chemotherapy regimen, to which only a fraction of patients respond and are physically able to withstand. However, the advent of deep genetic sequencing has led to the discovery of a number of mutational lesions targetable by small-molecule inhibitors, which more patients can tolerate. This dissertation demonstrates that AML drives in vivo T cell exhaustion, which is coordinated by multiple T cell receptor (TCR) activated transcription factors and BET proteins.</abstract>
  <pub-location/>
  <publisher>Oregon Health and Science University</publisher>
  <issn/>
  <isbn/>
  <custom3/>
  <custom7/>
  <notes/>
  <work-type>Dissertation</work-type>
  <electronic-resource-num>10.6083/z890rt88b</electronic-resource-num>
  <urls>
    <related-urls>
      <url>https://digitalcollections.ohsu.edu/record/9487/files/Romine.Kyle.2022.pdf</url>
    </related-urls>
  </urls>
  <language/>
</record>

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