6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Uncertainty quantification on a spatial Markov-chain model for the progression of skin cancer

      research-article
      1 , , 2
      Journal of Mathematical Biology
      Springer Berlin Heidelberg
      60J20, 65C05, 65C40

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A spatial Markov-chain model is formulated for the progression of skin cancer. The model is based on the division of the computational domain into nodal points, that can be in a binary state: either in ‘cancer state’ or in ‘non-cancer state’. The model assigns probabilities for the non-reversible transition from ‘non-cancer’ state to the ‘cancer state’ that depend on the states of the neighbouring nodes. The likelihood of transition further depends on the life burden intensity of the UV-rays that the skin is exposed to. The probabilistic nature of the process and the uncertainty in the input data is assessed by the use of Monte Carlo simulations. A good fit between experiments on mice and our model has been obtained.

          Related collections

          Most cited references23

          • Record: found
          • Abstract: not found
          • Article: not found

          Multilevel Monte Carlo methods and applications to elliptic PDEs with random coefficients

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Simulated brain tumor growth dynamics using a three-dimensional cellular automaton.

            We have developed a novel and versatile three-dimensional cellular automaton model of brain tumor growth. We show that macroscopic tumor behavior can be realistically modeled using microscopic parameters. Using only four parameters, this model simulates Gompertzian growth for a tumor growing over nearly three orders of magnitude in radius. It also predicts the composition and dynamics of the tumor at selected time points in agreement with medical literature. We also demonstrate the flexibility of the model by showing the emergence, and eventual dominance, of a second tumor clone with a different genotype. The model incorporates several important and novel features, both in the rules governing the model and in the underlying structure of the model. Among these are a new definition of how to model proliferative and non-proliferative cells, an isotropic lattice, and an adaptive grid lattice. Copyright 2000 Academic Press.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A cellular automaton model for tumour growth in inhomogeneous environment.

              Most of the existing mathematical models for tumour growth and tumour-induced angiogenesis neglect blood flow. This is an important factor on which both nutrient and metabolite supply depend. In this paper we aim to address this shortcoming by developing a mathematical model which shows how blood flow and red blood cell heterogeneity influence the growth of systems of normal and cancerous cells. The model is developed in two stages. First we determine the distribution of oxygen in a native vascular network, incorporating into our model features of blood flow and vascular dynamics such as structural adaptation, complex rheology and red blood cell circulation. Once we have calculated the oxygen distribution, we then study the dynamics of a colony of normal and cancerous cells, placed in such a heterogeneous environment. During this second stage, we assume that the vascular network does not evolve and is independent of the dynamics of the surrounding tissue. The cells are considered as elements of a cellular automaton, whose evolution rules are inspired by the different behaviour of normal and cancer cells. Our aim is to show that blood flow and red blood cell heterogeneity play major roles in the development of such colonies, even when the red blood cells are flowing through the vasculature of normal, healthy tissue.
                Bookmark

                Author and article information

                Contributors
                F.J.Vermolen@tudelft.nl
                ilkka.polonen@jyu.fi
                Journal
                J Math Biol
                J Math Biol
                Journal of Mathematical Biology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0303-6812
                1432-1416
                19 December 2019
                19 December 2019
                2020
                : 80
                : 3
                : 545-573
                Affiliations
                [1 ]GRID grid.5292.c, ISNI 0000 0001 2097 4740, Delft Institute of Applied Mathematics, , Delft University of Technology, ; Delft, The Netherlands
                [2 ]Faculty of Information Technology, University of Jyväskulä, 40014 Jyvaskyla, Finland
                Author information
                http://orcid.org/0000-0003-2212-1711
                Article
                1367
                10.1007/s00285-019-01367-y
                7028824
                31858196
                4da7d220-bf07-4845-844f-4ec7d81058a0
                © The Author(s) 2019

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 28 September 2018
                : 14 March 2019
                Funding
                Funded by: Delft University of Technology
                Categories
                Article
                Custom metadata
                © Springer-Verlag GmbH Germany, part of Springer Nature 2020

                Quantitative & Systems biology
                60j20,65c05,65c40
                Quantitative & Systems biology
                60j20, 65c05, 65c40

                Comments

                Comment on this article