ArticleThe European physical journal. E, Soft matter2019
Agent-based model of multicellular tumor spheroid evolution including cell metabolism.
Article in The European physical journal. E, Soft matter, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Comparison of volumetric dynamic optical coherence tomography with biological methods for evaluation of radiation effects in prostate tumor spheroids.Journal of biomedical optics · 2026Article
- Novel Diffuse Midline Glioma-on-Chip Recapitulating Tumor Biophysical Microenvironment to Assess the Heterogeneity of Response to Therapies.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Hybrid computational models of multicellular tumour growth considering glucose metabolism.Computational and structural biotechnology journal · 2023Review
- Bayesian calibration of a stochastic, multiscale agent-based model for predicting in vitro tumor growth.PLoS computational biology · 2021Article
- Mathematical modelling reveals cellular dynamics within tumour spheroids.PLoS computational biology · 2020Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Computational models aiming at the spatio-temporal description of cancer evolution are a suitable framework for testing biological hypotheses from experimental data, and generating new ones. Building on our recent work (J. Theor. Biol. 389, 146 (2016)) we develop a 3D agent-based model, capable of tracking hundreds of thousands of interacting cells, over time scales ranging from seconds to years. Cell dynamics is driven by a Monte Carlo solver, incorporating partial differential equations to describe chemical pathways and the activation/repression of "genes", leading to the up- or down-regulation of specific cell markers. Each cell-agent of different kind (stem, cancer, stromal etc.) runs through its cycle, undergoes division, can exit to a dormant, senescent, necrotic state, or apoptosis, according to the inputs from its systemic network. The basic network at this stage describes glucose/oxygen/ATP cycling, and can be readily extended to cancer-cell specific markers. Eventual accumulation of chemical/radiation damage to each cell's DNA is described by a Markov chain of internal states, and by a damage-repair network, whose evolution is linked to the cell systemic network. Aimed at a direct comparison with experiments of tumorsphere growth from stem cells, the present model will allow to quantitatively study the role of transcription factors involved in the reprogramming and variable radio-resistance of simulated cancer-stem cells, evolving in a realistic computer simulation of a growing multicellular tumorsphere.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.