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  <identifier identifierType="DOI">10.18453/rosdok_id00005667</identifier>
  <creators>
    <creator>
      <creatorName nameType="Personal">Dhar, Prabir</creatorName>
      <givenName>Prabir</givenName>
      <familyName>Dhar</familyName>
      <nameIdentifier nameIdentifierScheme="GND" schemeURI="http://d-nb.info/gnd/">http://d-nb.info/gnd/1412077737</nameIdentifier>
    </creator>
  </creators>
  <titles>
    <title>E2F1-induced IL6 mediates cancer-immune cell crosstalk by modulating T cell response in tumor microenvironment that regulates metastatic properties in melanoma</title>
  </titles>
  <publisher>Universität Rostock</publisher>
  <publicationYear>2025</publicationYear>
  <resourceType resourceTypeGeneral="Text" />
  <subjects>
    <subject xml:lang="en" schemeURI="http://dewey.info/" subjectScheme="dewey">570 Life science</subject>
    <subject xml:lang="en" schemeURI="http://dewey.info/" subjectScheme="dewey">610 Medical sciences Medicine</subject>
  </subjects>
  <dates>
    <date dateType="Created">2025</date>
  </dates>
  <language>en</language>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="PURL">https://purl.uni-rostock.de/rosdok/id00005667</alternateIdentifier>
    <alternateIdentifier alternateIdentifierType="URN">urn:nbn:de:gbv:28-rosdok_id00005667-5</alternateIdentifier>
  </alternateIdentifiers>
  <descriptions>
    <description descriptionType="Abstract">In melanoma, E2F1 plays a key role as a regulator of tumor progression. This study identifies a novel gene regulatory network by which E2F1-induced factor IL6 modulates the melanoma microenvironment by altering CD4+ or CD8+ T cell responses. In neighboring CD4+ and CD8+ T cells, IL6 induced the expression of IL10 as well as changes in the secretome profile. In combination with clinical data from TCGA, this study suggests a new melanoma cancer-specific molecular signature, low-E2F1/high-IL10/low-IL6, which is associated with a favourable clinical outcome.</description>
  </descriptions>
</resource>
