% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Kaczorowski:128859,
      author       = {A. Kaczorowski and K. Hammer$^*$ and L. Liu and S.
                      Villhauer and C. Nwaeburu and P. Fan and Z. Zhao and J.
                      Gladkich and W. Groß and D. Nettelbeck$^*$ and I. Herr},
      title        = {{D}elivery of improved oncolytic adenoviruses by
                      mesenchymal stromal cells for elimination of tumorigenic
                      pancreatic cancer cells.},
      journal      = {OncoTarget},
      volume       = {7},
      number       = {8},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-04872},
      pages        = {9046 - 9059},
      year         = {2016},
      abstract     = {Pancreatic ductal adenocarcinoma (PDA) is one of the most
                      aggressive malignancies and has poor therapeutic options. We
                      evaluated improved oncolytic adenoviruses (OAds), in which
                      the adenoviral gene E1B19K was deleted or a TRAIL transgene
                      was inserted. Bone marrow mesenchymal stromal cells (MSCs)
                      served as carriers for protected and tumor-specific virus
                      transfers. The infection competence, tumor migration, and
                      oncolysis were measured in cancer stem cell (CSC) models of
                      primary and established tumor cells and in tumor xenografts.
                      All OAds infected and lysed CSCs and prevented colony
                      formation. MSCs migrated into PDA spheroids without impaired
                      homing capacity. Xenotransplantation of non-infected PDA
                      cells mixed with infected tumor cells strongly reduced the
                      tumor volume and the expression of the proliferation marker
                      Ki67 along with a necrotic morphology. Adenoviral capsid
                      protein was detected in tumor xenograft tissue after
                      intravenous injection of infected MSCs, but not in normal
                      tissue, implying tumor-specific migration. Likewise, direct
                      in vivo treatment correlated with a strongly reduced tumor
                      volume, lower expression of Ki67 and CD24, and enhanced
                      activity of caspase 3. These data demonstrate that the
                      improved OAds induced efficient oncolysis with the OAd-TRAIL
                      as most promising candidate for future clinical
                      application.},
      keywords     = {Adaptor Proteins, Signal Transducing (NLM Chemicals) /
                      Antigens, CD24 (NLM Chemicals) / CD24 protein, human (NLM
                      Chemicals) / Capsid Proteins (NLM Chemicals) / Ki-67 Antigen
                      (NLM Chemicals) / Caspase 3 (NLM Chemicals)},
      cin          = {F110},
      ddc          = {610},
      cid          = {I:(DE-He78)F110-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26824985},
      pmc          = {pmc:PMC4891025},
      doi          = {10.18632/oncotarget.7031},
      url          = {https://inrepo02.dkfz.de/record/128859},
}