On a mathematical model of bone marrow metastatic niche

Ana Isabel Muñoz; J. Ignacio Tello; Ana Isabel Muñoz; J. Ignacio Tello

doi:10.3934/mbe.2017019

Mathematical Biosciences and Engineering

2017, Volume 14, Issue 1: 289-304. doi: 10.3934/mbe.2017019

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On a mathematical model of bone marrow metastatic niche

Ana Isabel Muñoz ¹,
J. Ignacio Tello ^{2,3
,
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1.
Departamento de Matemática Aplicada, Ciencia e Ingeniería de Materiales y Tecnología Electrónica, ESCET, Universidad Rey Juan Carlos, E28933, Móstoles, Madrid, Spain
2.
Depto. Matemática Aplicada a las T.I.C. ETSI Sistemas Informáticos, Universidad Politécnica de Madrid. Madrid 28031, Spain
3.
Centro de Simulación Computacional, Universidad Politécnica de Madrid. Boadilla del Monte, Madrid 28660, Spain

Received: 23 November 2015 Accepted: 14 June 2016 Published: 01 January 2017
MSC : Primary: 35Q92; Secondary: 35R60

We propose a mathematical model to describe tumor cells movement towards a metastasis location into the bone marrow considering the influence of chemotaxis inhibition due to the action of a drug. The model considers the evolution of the signaling molecules CXCL-12 secreted by osteoblasts (bone cells responsible of the mineralization of the bone) and PTHrP (secreted by tumor cells) which activates osteoblast growth. The model consists of a coupled system of second order PDEs describing the evolution of CXCL-12 and PTHrP, an ODE of logistic type to model the Osteoblasts density and an extra equation for each cancer cell. We also simulate the system to illustrate the qualitative behavior of the solutions. The numerical method of resolution is also presented in detail.
- Mathematical modeling of cancer,
- hematopoietic niche,
- osteoblast,
- CXCL-12,
- PTHrP,
- FEM
Citation: Ana Isabel Muñoz, J. Ignacio Tello. On a mathematical model of bone marrow metastatic niche[J]. Mathematical Biosciences and Engineering, 2017, 14(1): 289-304. doi: 10.3934/mbe.2017019

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Abstract

We propose a mathematical model to describe tumor cells movement towards a metastasis location into the bone marrow considering the influence of chemotaxis inhibition due to the action of a drug. The model considers the evolution of the signaling molecules CXCL-12 secreted by osteoblasts (bone cells responsible of the mineralization of the bone) and PTHrP (secreted by tumor cells) which activates osteoblast growth. The model consists of a coupled system of second order PDEs describing the evolution of CXCL-12 and PTHrP, an ODE of logistic type to model the Osteoblasts density and an extra equation for each cancer cell. We also simulate the system to illustrate the qualitative behavior of the solutions. The numerical method of resolution is also presented in detail.

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