ArticleTheoretical biology & medical modelling2007
Simulating non-small cell lung cancer with a multiscale agent-based model.
Article in Theoretical biology & medical modelling, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed.
- Evolutionary rescue model informs strategies for driving cancer cell populations to extinction.bioRxiv : the preprint server for biology · 2025Article
- A comprehensive review of computational cell cycle models in guiding cancer treatment strategies.NPJ systems biology and applications · 2024Review
- Hybrid Cellular Automata Modeling Reveals the Effects of Glucose Gradients on Tumour Spheroid Growth.Cancers · 2023Article
- A circuit for secretion-coupled cellular autonomy in multicellular eukaryotic cells.Molecular systems biology · 2023Article
- Data-driven spatio-temporal modelling of glioblastoma.Royal Society open science · 2023Review
- A multi-layered hybrid model for cancer cell invasion.Medical & biological engineering & computing · 2022Article
- Navigating Multi-Scale Cancer Systems Biology Towards Model-Driven Clinical Oncology and Its Applications in Personalized Therapeutics.Frontiers in oncology · 2021Review
- Role of PARP1-mediated autophagy in EGFR-TKI resistance in non-small cell lung cancer.Scientific reports · 2020Article
- Multiscale Model Identifies Improved Schedule for Treatment of Acute Myeloid Leukemia In Vitro With the Mcl-1 Inhibitor AZD5991.CPT: pharmacometrics & systems pharmacology · 2020Article
- Multi-scale models of lung fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- A Multiscale Agent-Based Model of Ductal Carcinoma In Situ.IEEE transactions on bio-medical engineering · 2020Article
- The road to ERK activation: Do neurons take alternate routes?Cellular signalling · 2020Review
- Data-driven analysis of a mechanistic model of CAR T cell signaling predicts effects of cell-to-cell heterogeneity.Journal of theoretical biology · 2020Article
- Three-dimensional tumor growth in time-varying chemical fields: a modeling framework and theoretical study.BMC bioinformatics · 2019Article
- Dynamic Targeting in Cancer Treatment.Frontiers in physiology · 2019Article
- A HYBRID THREE-SCALE MODEL OF TUMOR GROWTH.Mathematical models & methods in applied sciences : M3AS · 2018Article
- Article
- The tumor as an organ: comprehensive spatial and temporal modeling of the tumor and its microenvironment.BMC bioinformatics · 2016Article
- A computational model of invasive aspergillosis in the lung and the role of iron.BMC systems biology · 2016Article
- Integrated PK-PD and agent-based modeling in oncology.Journal of pharmacokinetics and pharmacodynamics · 2015Review
Corrections and comments
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4 authors.
Funding
Abstract
backgroundThe epidermal growth factor receptor (EGFR) is frequently overexpressed in many cancers, including non-small cell lung cancer (NSCLC). In silico modeling is considered to be an increasingly promising tool to add useful insights into the dynamics of the EGFR signal transduction pathway. However, most of the previous modeling work focused on the molecular or the cellular level only, neglecting the crucial feedback between these scales as well as the interaction with the heterogeneous biochemical microenvironment.
resultsWe developed a multiscale model for investigating expansion dynamics of NSCLC within a two-dimensional in silico microenvironment. At the molecular level, a specific EGFR-ERK intracellular signal transduction pathway was implemented. Dynamical alterations of these molecules were used to trigger phenotypic changes at the cellular level. Examining the relationship between extrinsic ligand concentrations, intrinsic molecular profiles and microscopic patterns, the results confirmed that increasing the amount of available growth factor leads to a spatially more aggressive cancer system. Moreover, for the cell closest to nutrient abundance, a phase-transition emerges where a minimal increase in extrinsic ligand abolishes the proliferative phenotype altogether.
conclusionOur in silico results indicate that in NSCLC, in the presence of a strong extrinsic chemotactic stimulus (and depending on the cell's location) downstream EGFR-ERK signaling may be processed more efficiently, thereby yielding a migration-dominant cell phenotype and overall, an accelerated spatio-temporal expansion rate.
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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.