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Highly desmoplastic and immune-desert phenotypes of pancreatic cancer remain two major hurdles that attenuate the efficacy of conventional treatment (radiotherapy and chemotherapy) and immunotherapeutic (immune checkpoint inhibitors and chimeric antigen receptor T cells).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>\n                      To overcome these hurdles, an oncolytic adenovirus (oAd) co-expressing interleukin-12, granulocyte macrophage colony-stimulating factor, and relaxin (HY-oAd) was investigated in combination with programmed death-ligand 1 (PD-L1)-targeted RIT (lutetium-177-labeled atezolizumab (\n                      <jats:sup>177<\/jats:sup>\n                      Lu-aPD-L1)).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      HY-oAd treatment was shown to elevate PD-L1 expression level and promoted degradation of extracellular matrix of pancreatic tumors, resulting in increased aPD-L1 or\n                      <jats:sup>64<\/jats:sup>\n                      Cu-aPD-L1 accumulation in tumor tissues. HY-oAd in combination with either aPD-L1 or\n                      <jats:sup>177<\/jats:sup>\n                      Lu-aPD-L1 (HY-oAd+aPD-L1 or HY-oAd+\n                      <jats:sup>177<\/jats:sup>\n                      Lu-aPD-L1, respectively) elicited more potent antitumor effect against the pancreatic tumors than respective monotherapy in both subcutaneous and orthotopic pancreatic tumor models. The potent antitumor effect of HY-oAd+aPD-L1 combination therapy was due to superior intratumoral infiltration and activation of dendritic cells and CD4\n                      <jats:sup>+<\/jats:sup>\n                      or CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells over the respective monotherapy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Collectively, our findings demonstrate that HY-oAd can enhance intratumoral accumulation of\n                      <jats:sup>177<\/jats:sup>\n                      Lu-aPD-L1 in a multifaceted manner to elicit synergistic antitumor immune response against desmoplastic and poorly immunogenic pancreatic tumors.\n                    <\/jats:p>\n                  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