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@ARTICLE{Larribre:142072,
      author       = {L. Larribère$^*$ and S. Kuphal and C. Sachpekidis$^*$ and
                      L. Hüser$^*$ and A. Bosserhoff and J. Utikal$^*$},
      collaboration = {S. Sachindra$^*$},
      title        = {{T}argeted {T}herapy-{R}esistant {M}elanoma {C}ells
                      {A}cquire {T}ranscriptomic {S}imilarities with {H}uman
                      {M}elanoblasts.},
      journal      = {Cancers},
      volume       = {10},
      number       = {11},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2018-02302},
      pages        = {451},
      year         = {2018},
      abstract     = {The mechanisms of adaptive and acquired drug resistance in
                      tumors are not completely understood. So far, gene
                      amplifications or mutations, leading to the reactivation of
                      the MAPK or PI3K pathways have been described. In this
                      study, we used two different methods to generate human
                      melanoblasts: (1) via differentiation from induced
                      pluripotent stem cells (iPSCs) and (2) via dedifferentiation
                      from melanocytes. The melanoblast transcriptomes were then
                      compared to the transcriptome of MAPK inhibitor-resistant
                      melanoma cells. We observed that the expression of genes
                      associated with cell cycle control, DNA damage control,
                      metabolism, and cancer was altered in both melanoblast
                      populations and in both adaptive and acquired resistant
                      melanoma samples, compared to drug-sensitive samples.
                      However, genes involved in antigen presentation and cellular
                      movement were only regulated in the melanoblast populations
                      and in the acquired resistant melanoma samples, compared to
                      the drug-sensitive samples. Moreover, melanocyte-derived
                      melanoblasts and adaptive resistant melanoma samples were
                      characterized by different expression levels of certain
                      transcription factors or genes involved in the CDK5 pathway.
                      In conclusion, we show here that in vitro models of human
                      melanoblasts are very important tools to comprehend the
                      expression profiles of drug-resistant melanoma.},
      cin          = {G300 / E060},
      ddc          = {610},
      cid          = {I:(DE-He78)G300-20160331 / I:(DE-He78)E060-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30453548},
      pmc          = {pmc:PMC6265976},
      doi          = {10.3390/cancers10110451},
      url          = {https://inrepo02.dkfz.de/record/142072},
}