<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE219174" accession="SRP438044">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP438044</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA907322</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE219174</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Cancer Cells Resistant to Immune Checkpoint Blockade Acquire Interferon-Associated Epigenetic Memory to Sustain T Cell Dysfunction (ATAC-Seq I)</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>We show that across human and/or mouse tumors immune dysfunction is associated with cancer cells acquiring epigenetic features of inflammatory memory. Here, inflammatory memory domains, many of which are initiated by chronic IFNG, are established by STAT1 and IRF3 and link H3K4me1-marked chromatin accessibility to increased expression of a subset of IFN-stimulated genes (ISGs). Overall design: ATAC-Seq</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE219174</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA907320</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
