A Multiscale Mathematical Model of Tumour Invasive Growth

Autor: Lu Peng, Mark A. J. Chaplain, Dumitru Trucu, Ping Lin, Alastair M. Thompson
Přispěvatelé: University of St Andrews. Applied Mathematics
Rok vydání: 2017
Předmět:
0301 basic medicine
QH301 Biology
Dynamical Systems (math.DS)
uPA system
Extracellular matrix
Multiscale modelling
0302 clinical medicine
Tumor Microenvironment
Fibrinolysin
Mathematics - Dynamical Systems
Tissues and Organs (q-bio.TO)
QA
General Environmental Science
education.field_of_study
Chemistry
General Neuroscience
Proteolytic enzymes
Extracellular Matrix
Cell biology
Computational Theory and Mathematics
030220 oncology & carcinogenesis
General Agricultural and Biological Sciences
Algorithms
medicine.drug
Cell type
General Mathematics
Immunology
Population
NDAS
Cancer invasion
Models
Biological
General Biochemistry
Genetics and Molecular Biology
RC0254
QH301
03 medical and health sciences
SDG 3 - Good Health and Well-being
FOS: Mathematics
medicine
Humans
Computer Simulation
Neoplasm Invasiveness
QA Mathematics
Quantitative Biology - Populations and Evolution
education
Pharmacology
Urokinase
RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Populations and Evolution (q-bio.PE)
Cancer
Quantitative Biology - Tissues and Organs
Mathematical Concepts
medicine.disease
Urokinase-Type Plasminogen Activator
030104 developmental biology
The Hallmarks of Cancer
FOS: Biological sciences
Cancer cell
Zdroj: Bulletin of Mathematical Biology. 79:389-429
ISSN: 1522-9602
0092-8240
Popis: Known as one of the hallmarks of cancer (Hanahan and Weinberg in Cell 100:57–70, 2000) cancer cell invasion of human body tissue is a complicated spatio-temporal multiscale process which enables a localised solid tumour to transform into a systemic, metastatic and fatal disease. This process explores and takes advantage of the reciprocal relation that solid tumours establish with the extracellular matrix (ECM) components and other multiple distinct cell types from the surrounding microenvironment. Through the secretion of various proteolytic enzymes such as matrix metalloproteinases or the urokinase plasminogen activator (uPA), the cancer cell population alters the configuration of the surrounding ECM composition and overcomes the physical barriers to ultimately achieve local cancer spread into the surrounding tissue. The active interplay between the tissue-scale tumour dynamics and the molecular mechanics of the involved proteolytic enzymes at the cell scale underlines the biologically multiscale character of invasion and raises the challenge of modelling this process with an appropriate multiscale approach. In this paper, we present a new two-scale moving boundary model of cancer invasion that explores the tissue-scale tumour dynamics in conjunction with the molecular dynamics of the urokinase plasminogen activation system. Building on the multiscale moving boundary method proposed in Trucu et al. (Multiscale Model Simul 11(1):309–335, 2013), the modelling that we propose here allows us to study the changes in tissue-scale tumour morphology caused by the cell-scale uPA microdynamics occurring along the invasive edge of the tumour. Our computational simulation results demonstrate a range of heterogeneous dynamics which are qualitatively similar to the invasive growth patterns observed in a number of different types of cancer, such as the tumour infiltrative growth patterns discussed in Ito et al. (J Gastroenterol 47:1279–1289, 2012). Postprint
Databáze: OpenAIRE
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