Academic Journal

Multiscale Modeling of Spheroid Tumors: Effect of Nutrient Availability on Tumor Evolution

Bibliographic Details
Title: Multiscale Modeling of Spheroid Tumors: Effect of Nutrient Availability on Tumor Evolution
Authors: Rosenbauer, Jakob, Berghoff, Marco, Glazier, James A., Schug, Alexander
Superior Title: The Journal of Physical Chemistry B, 127 (16), 3607–3615 ; ISSN: 1520-6106, 1089-5647, 1520-5207
Publisher Information: American Chemical Society
Publication Year: 2023
Collection: KITopen (Karlsruhe Institute of Technologie)
Subject Terms: ddc:004, DATA processing & computer science, info:eu-repo/classification/ddc/004
Description: 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.
Document Type: article in journal/newspaper
File Description: application/pdf
Language: English
ISBN: 978-1-00-015801-4
1-00-015801-2
Relation: info:eu-repo/semantics/altIdentifier/wos/000967258200001; info:eu-repo/semantics/altIdentifier/issn/1520-6106; info:eu-repo/semantics/altIdentifier/issn/1089-5647; info:eu-repo/semantics/altIdentifier/issn/1520-5207; https://publikationen.bibliothek.kit.edu/1000158012; https://publikationen.bibliothek.kit.edu/1000158012/150677716; https://doi.org/10.5445/IR/1000158012
DOI: 10.5445/IR/1000158012
Availability: https://doi.org/10.5445/IR/1000158012
https://doi.org/10.1021/acs.jpcb.2c08114
https://publikationen.bibliothek.kit.edu/1000158012
https://publikationen.bibliothek.kit.edu/1000158012/150677716
Rights: https://creativecommons.org/licenses/by/4.0/deed.de ; info:eu-repo/semantics/openAccess
Accession Number: edsbas.B76C5C76
Database: BASE
Description
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