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@ARTICLE{Rosenbauer:1006629,
      author       = {Rosenbauer, Jakob and Berghoff, Marco and Glazier, James A.
                      and Schug, Alexander},
      title        = {{M}ultiscale {M}odeling of {S}pheroid {T}umors: {E}ffect of
                      {N}utrient {A}vailability on {T}umor {E}volution},
      journal      = {The journal of physical chemistry / B},
      volume       = {127},
      number       = {16},
      issn         = {1520-6106},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {FZJ-2023-01762},
      pages        = {3607–3615},
      year         = {2023},
      abstract     = {Recent years have revealed a large number of complex
                      mechanisms and interactions that drive the development of
                      malignant tumors. Tumor evolution is a framework that
                      explains tumor development as a process driven by survival
                      of the fittest, with tumor cells of different properties
                      competing for limited available resources. To predict the
                      evolutionary trajectory of a tumor, knowledge of how
                      cellular properties influence the fitness of a subpopulation
                      in the context of the microenvironment is required and is
                      often inaccessible. Computational multiscale-modeling of
                      tissues enables the observation of the full trajectory of
                      each cell within the tumor environment. Here, we model a 3D
                      spheroid tumor with subcellular resolution. The fitness of
                      individual cells and the evolutionary behavior of the tumor
                      are quantified and linked to cellular and environmental
                      parameters. The fitness of cells is solely influenced by
                      their position in the tumor, which in turn is influenced by
                      the two variable parameters of our model: cell–cell
                      adhesion and cell motility. We observe the influence of
                      nutrient independence and static and dynamically changing
                      nutrient availability on the evolutionary trajectories of
                      heterogeneous tumors in a high-resolution computational
                      model. Regardless of nutrient availability, we find a
                      fitness advantage of low-adhesion cells, which are favorable
                      for tumor invasion. We find that the introduction of
                      nutrient-dependent cell division and death accelerates the
                      evolutionary speed. The evolutionary speed can be increased
                      by fluctuations in nutrients. We identify a distinct
                      frequency domain in which the evolutionary speed increases
                      significantly over a tumor with constant nutrient supply.
                      The findings suggest that an unstable supply of nutrients
                      can accelerate tumor evolution and, thus, the transition to
                      malignancy.},
      cin          = {JSC},
      ddc          = {530},
      cid          = {I:(DE-Juel1)JSC-20090406},
      pnm          = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
                      (SDLs) and Research Groups (POF4-511) / Forschergruppe Schug
                      $(hkf6_20200501)$},
      pid          = {G:(DE-HGF)POF4-5111 / $G:(DE-Juel1)hkf6_20200501$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37011021},
      UT           = {WOS:000967258200001},
      doi          = {10.1021/acs.jpcb.2c08114},
      url          = {https://juser.fz-juelich.de/record/1006629},
}