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@ARTICLE{Zhang:127854,
      author       = {Y. Zhang$^*$ and L. Liu$^*$ and P. Fan$^*$ and N. Bauer$^*$
                      and J. Gladkich$^*$ and E. Ryschich and A. V. Bazhin and N.
                      A. Giese and O. Strobel and T. Hackert and U. Hinz and W.
                      Gross$^*$ and F. Fortunato and I. Herr$^*$},
      title        = {{A}spirin counteracts cancer stem cell features,
                      desmoplasia and gemcitabine resistance in pancreatic
                      cancer.},
      journal      = {OncoTarget},
      volume       = {6},
      number       = {12},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-03876},
      pages        = {9999 - 10015},
      year         = {2015},
      abstract     = {Pancreatic ductal adenocarcinoma (PDA) is characterized by
                      an extremely poor prognosis. An inflammatory
                      microenvironment triggers the pronounced desmoplasia, the
                      selection of cancer stem-like cells (CSCs) and therapy
                      resistance. The anti-inflammatory drug aspirin is suggested
                      to lower the risk for PDA and to improve the treatment,
                      although available results are conflicting and the effect of
                      aspirin to CSC characteristics and desmoplasia in PDA has
                      not yet been investigated. We characterized the influence of
                      aspirin on CSC features, stromal reactions and gemcitabine
                      resistance. Four established and 3 primary PDA cell lines,
                      non-malignant cells, 3 patient tumor-derived CSC-enriched
                      spheroidal cultures and tissues from patients who did or did
                      not receive aspirin before surgery were analyzed using MTT
                      assays, flow cytometry, colony and spheroid formation
                      assays, Western blot analysis, antibody protein arrays,
                      electrophoretic mobility shift assays (EMSAs),
                      immunohistochemistry and in vivo xenotransplantation.
                      Aspirin significantly induced apoptosis and reduced the
                      viability, self-renewal potential, and expression of
                      proteins involved in inflammation and stem cell signaling.
                      Aspirin also reduced the growth and invasion of tumors in
                      vivo, and it significantly prolonged the survival of mice
                      with orthotopic pancreatic xenografts in combination with
                      gemcitabine. This was associated with a decreased expression
                      of markers for progression, inflammation and desmoplasia.
                      These findings were confirmed in tissue samples obtained
                      from patients who had or had not taken aspirin before
                      surgery. Importantly, aspirin sensitized cells that were
                      resistant to gemcitabine and thereby enhanced the
                      therapeutic efficacy. Aspirin showed no obvious toxic
                      effects on normal cells, chick embryos or mice. These
                      results highlight aspirin as an effective, inexpensive and
                      well-tolerated co-treatment to target inflammation,
                      desmoplasia and CSC features PDA.},
      keywords     = {Biomarkers, Tumor (NLM Chemicals) / Deoxycytidine (NLM
                      Chemicals) / gemcitabine (NLM Chemicals) / Aspirin (NLM
                      Chemicals)},
      cin          = {G403},
      ddc          = {610},
      cid          = {I:(DE-He78)G403-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25846752},
      pmc          = {pmc:PMC4496413},
      doi          = {10.18632/oncotarget.3171},
      url          = {https://inrepo02.dkfz.de/record/127854},
}