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                <h1 class="mt-0 mb-3 mb-lg-5">Functional malignant cell heterogeneity in pancreatic neuroendocrine tumors revealed by targeting of PDGF-DD.
                </h1>
                <h2 class="h6">Författare</h2>
                <p>
                    <a href="#">Eliane Cortez</a><br>
                    <a href="#">Hanna Gladh</a><br>
                    <a href="#">Sebastian Braun</a><br>
                    <a href="#">Matteo Bocci</a><br> Eugenia Cordero<br> Niklas K Björkström<br> Hideki Miyazaki<br> Iacovos P Michael<br> Ulf Eriksson<br> Erika Folestad<br> Kristian Pietras
                </p>
                <h2>Sammanfattning på Engelska</h2>
                <p>Intratumoral heterogeneity is an inherent feature of most human cancers and has profound implications for cancer therapy. As a result, there is an emergent need to explore previously unmapped mechanisms regulating distinct subpopulations
                    of tumor cells and to understand their contribution to tumor progression and treatment response. Aberrant platelet-derived growth factor receptor beta (PDGFRβ) signaling in cancer has motivated the development of several antagonists
                    currently in clinical use, including imatinib, sunitinib, and sorafenib. The discovery of a novel ligand for PDGFRβ, platelet-derived growth factor (PDGF)-DD, opened the possibility of a previously unidentified signaling pathway involved
                    in tumor development. However, the precise function of PDGF-DD in tumor growth and invasion remains elusive. Here, making use of a newly generated Pdgfd knockout mouse, we reveal a functionally important malignant cell heterogeneity
                    modulated by PDGF-DD signaling in pancreatic neuroendocrine tumors (PanNET).</p>
                <p>Our analyses demonstrate that tumor growth was delayed in the absence of signaling by PDGF-DD. Surprisingly, ablation of PDGF-DD did not affect the vasculature or stroma of PanNET; instead, we found that PDGF-DD stimulated bulk tumor cell
                    proliferation by induction of paracrine mitogenic signaling between heterogeneous malignant cell clones, some of which expressed PDGFRβ. The presence of a subclonal population of tumor cells characterized by PDGFRβ expression was further
                    validated in a cohort of human PanNET. In conclusion, we demonstrate a previously unrecognized heterogeneity in PanNET characterized by signaling through the PDGF-DD/PDGFRβ axis.</p>
            </div>
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                    <p>
                        <strong>Avdelning/ar:</strong><br>
                        <a href="#">Avdelningen för translationell cancerforskning</a><br>
                        <a href="#">Experimentell onkologi</a>
                    </p>
                    <p><strong>Publiceringsår:</strong> 2016</p>
                    <p><strong>Språk:</strong> Engelska</p>
                    <p><strong>Sidor:</strong> 864-873</p>
                    <p><strong>Publikation/Tidskrift/Serie:</strong> Proceedings of the National Academy of Sciences</p>
                    <p><strong>Volym:</strong> 113</p>
                    <p><strong>Nummer:</strong> 7</p>
                    <p><strong>Fulltext:</strong><br>
                        <a href="#">Tillgänglig som fulltext</a><br>
                        <a href="#">Nedladdningsstatistik</a></p>
                    <p>
                        <strong>Länkar:</strong><br>
                        <a href="#">Exempellänk</a>
                    </p>
                    <p><strong>Dokumenttyp:</strong> Artikel i tidskrift</p>
                    <p><strong>Förlag:</strong> National Acad Sciences</p>
                </div>

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                        <strong>Ämne</strong><br> Cancer and Oncology
                    </p>
                    <p>
                        <strong>Status</strong><br> Published
                    </p>
                    <p>
                        <strong>Forskningsgrupp</strong><br> Experimental oncology
                    </p>
                    <p>
                        <strong>ISBN/ISSN/Andra:</strong><br> ISSN: 1091-6490
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<main id="lunds-universitet" class="main">
  <div class="container">
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        <a href="#">This page in English</a>
      </div>
    </div>
    <div class="row">
      <div class="col-12 col-lg-8 mb-5 mb-lg-0">
        <h1 class="mt-0 mb-3 mb-lg-5">Functional malignant cell heterogeneity in pancreatic neuroendocrine tumors
          revealed by targeting of
          PDGF-DD.</h1>
        <h2 class="h6">Författare</h2>
        <p>
          <a href="#">Eliane Cortez</a><br>
          <a href="#">Hanna Gladh</a><br>
          <a href="#">Sebastian Braun</a><br>
          <a href="#">Matteo Bocci</a><br>
          Eugenia Cordero<br>
          Niklas K Björkström<br>
          Hideki Miyazaki<br>
          Iacovos P Michael<br>
          Ulf Eriksson<br>
          Erika Folestad<br>
          Kristian Pietras
        </p>
        <h2>Sammanfattning på Engelska</h2>
        <p>Intratumoral heterogeneity is an inherent feature of most human cancers and has profound implications for
          cancer therapy. As a result, there is an emergent need to explore previously unmapped mechanisms regulating
          distinct subpopulations of tumor cells and to understand their contribution to tumor progression and treatment
          response. Aberrant platelet-derived growth factor receptor beta (PDGFRβ) signaling in cancer has motivated the
          development of several antagonists currently in clinical use, including imatinib, sunitinib, and sorafenib.
          The discovery of a novel ligand for PDGFRβ, platelet-derived growth factor (PDGF)-DD, opened the possibility
          of a previously unidentified signaling pathway involved in tumor development. However, the precise function of
          PDGF-DD in tumor growth and invasion remains elusive. Here, making use of a newly generated Pdgfd knockout
          mouse, we reveal a functionally important malignant cell heterogeneity modulated by PDGF-DD signaling in
          pancreatic neuroendocrine tumors (PanNET).</p>
        <p>Our analyses demonstrate that tumor growth was delayed in the absence of signaling by PDGF-DD. Surprisingly,
          ablation of PDGF-DD did not affect the vasculature or stroma of PanNET; instead, we found that PDGF-DD
          stimulated bulk tumor cell proliferation by induction of paracrine mitogenic signaling between heterogeneous
          malignant cell clones, some of which expressed PDGFRβ. The presence of a subclonal population of tumor cells
          characterized by PDGFRβ expression was further validated in a cohort of human PanNET. In conclusion, we
          demonstrate a previously unrecognized heterogeneity in PanNET characterized by signaling through the
          PDGF-DD/PDGFRβ axis.</p>
      </div>
      <div class="col-12 col-lg-4 col-xl-3 offset-xl-1">
        <div class="infobox bg-copper-50">
          <p>
            <strong>Avdelning/ar:</strong><br>
            <a href="#">Avdelningen för translationell cancerforskning</a><br>
            <a href="#">Experimentell onkologi</a>
          </p>
          <p><strong>Publiceringsår:</strong> 2016</p>
          <p><strong>Språk:</strong> Engelska</p>
          <p><strong>Sidor:</strong> 864-873</p>
          <p><strong>Publikation/Tidskrift/Serie:</strong> Proceedings of the National Academy of Sciences</p>
          <p><strong>Volym:</strong> 113</p>
          <p><strong>Nummer:</strong> 7</p>
          <p><strong>Fulltext:</strong><br>
            <a href="#">Tillgänglig som fulltext</a><br>
            <a href="#">Nedladdningsstatistik</a></p>
          <p>
            <strong>Länkar:</strong><br>
            <a href="#">Exempellänk</a>
          </p>
          <p><strong>Dokumenttyp:</strong> Artikel i tidskrift</p>
          <p><strong>Förlag:</strong> National Acad Sciences</p>
        </div>

        <div class="infobox bg-sky-50">
          <p>
            <strong>Ämne</strong><br>
            Cancer and Oncology
          </p>
          <p>
            <strong>Status</strong><br>
            Published
          </p>
          <p>
            <strong>Forskningsgrupp</strong><br>
            Experimental oncology
          </p>
          <p>
            <strong>ISBN/ISSN/Andra:</strong><br>
            ISSN: 1091-6490
          </p>
        </div>
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