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@ARTICLE{Wang:298341,
      author       = {C. Wang$^*$ and N. Stöffler$^*$ and H. Liu$^*$},
      title        = {{L}aboratory-{E}ngineered {G}lioblastoma {O}rganoid
                      {C}ulture and {D}rug {S}creening.},
      journal      = {JoVE journal},
      volume       = {215},
      issn         = {1940-087X},
      address      = {Cambridge, MA},
      publisher    = {JoVE},
      reportid     = {DKFZ-2025-00245},
      pages        = {e67593},
      year         = {2025},
      note         = {#EA:A240#LA:A240#},
      abstract     = {Glioblastoma (GBM) is described as a group of highly
                      malignant primary brain tumors and stands as one of the most
                      lethal malignancies. The genetic and cellular
                      characteristics of GBM have been a focal point of ongoing
                      research, revealing that it is a group of heterogeneous
                      diseases with variations in RNA expression, DNA methylation,
                      or cellular composition. Despite the wealth of molecular
                      data available, the lack of transferable pre-clinic models
                      has limited the application of this information to disease
                      classification rather than treatment stratification.
                      Transferring the patients' genetic information into clinical
                      benefits and bridging the gap between detailed descriptions
                      of GBM, genotype-phenotype associations, and treatment
                      advancements remain significant challenges. In this context,
                      we present an advanced human GBM organoid model, the
                      Laboratory Engineered Glioblastoma Organoid (LEGO), and
                      illustrate its use in studying the genotype-phenotype
                      dependencies and screening potential drugs for GBM.
                      Utilizing this model, we have identified lipid metabolism
                      dysregulation as a critical milestone in GBM progression and
                      discovered that the microsomal triglyceride transfer protein
                      inhibitor Lomitapide shows promise as a potential treatment
                      for GBM.},
      keywords     = {Glioblastoma: genetics / Glioblastoma: pathology / Humans /
                      Organoids: metabolism / Organoids: drug effects / Brain
                      Neoplasms: genetics / Brain Neoplasms: pathology / Drug
                      Screening Assays, Antitumor: methods / Drug Evaluation,
                      Preclinical: methods},
      cin          = {A240},
      ddc          = {570},
      cid          = {I:(DE-He78)A240-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39868688},
      doi          = {10.3791/67593},
      url          = {https://inrepo02.dkfz.de/record/298341},
}