<?xml version="1.0" encoding="UTF-8"?>
<references>
<reference>
  <rt>Dissertation</rt>
  <a1>Lin, Hsin-Yun</a1>
  <t1>Identification of TLK/ASF1 as a novel pathway for mediating IL-1B-driven acute myeloid leukemia</t1>
  <ot/>
  <jf/>
  <sn/>
  <do>10.6083/4t64gn939</do>
  <vo/>
  <is/>
  <sp/>
  <op/>
  <ab>Genetic heterogeneity makes clinical interventions challenging for patients with acute myeloid leukemia (AML). Identifying and targeting common microenvironment-driven pathways should allow the development of effective therapies across AML genetic subtypes. Our laboratory has previously shown that the AML microenvironment is rich in proinflammatory cytokine interleukin-1B (IL-1B) and promotes the growth of AML progenitors. To elucidate the molecular underpinnings of IL-1B-driven AML progression, transcriptome analysis was performed and identified that ASF1B (anti-silencing function-1B) is one of the most differentially expressed genes in AML compared to healthy progenitors. This dissertation focuses on how ASF1B, and its regulator tousled-like kinase 2 (TLK2) contribute to AML cell growth and IL-1B-driven AML progression.</ab>
  <la/>
  <k1>mouse;
                asf1b protein;
                tousled like kinase 2;
                Interleukin-1;
                DNA Damage;
                Histone Chaperones;
                Leukemia, Myeloid, Acute;
                </k1>
  <pb>Oregon Health and Science University</pb>
  <pp/>
  <yr/>
  <ed/>
  <ul>https://digitalcollections.ohsu.edu/record/9954/files/Lin.HsinYun.2022.pdf;
	</ul>
</reference>

</references>