Yang2012 - cancer growth with angiogenesis

  public model
Model Identifier
BIOMD0000000796
Short description
The paper describes a model of tumor growth with angiogenesis. Created by COPASI 4.26 (Build 213) This model is described in the article: Mathematical modeling of solid cancer growth with angiogenesis Hyun M Yang Theoretical Biology and Medical Modelling 2012, 9:2 Abstract: Background: Cancer arises when within a single cell multiple malfunctions of control systems occur, which are, broadly, the system that promote cell growth and the system that protect against erratic growth. Additional systems within the cell must be corrupted so that a cancer cell, to form a mass of any real size, produces substances that promote the growth of new blood vessels. Multiple mutations are required before a normal cell can become a cancer cell by corruption of multiple growth-promoting systems. Methods: We develop a simple mathematical model to describe the solid cancer growth dynamics inducing angiogenesis in the absence of cancer controlling mechanisms. Results: The initial conditions supplied to the dynamical system consist of a perturbation in form of pulse: The origin of cancer cells from normal cells of an organ of human body. Thresholds of interacting parameters were obtained from the steady states analysis. The existence of two equilibrium points determine the strong dependency of dynamical trajectories on the initial conditions. The thresholds can be used to control cancer. Conclusions: Cancer can be settled in an organ if the following combination matches: better fitness of cancer cells, decrease in the efficiency of the repairing systems, increase in the capacity of sprouting from existing vascularization, and higher capacity of mounting up new vascularization. However, we show that cancer is rarely induced in organs (or tissues) displaying an efficient (numerically and functionally) reparative or regenerative mechanism. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.
Format
SBML (L3V1)
Related Publication
  • Mathematical modeling of solid cancer growth with angiogenesis.
  • Yang HM
  • Theoretical biology & medical modelling , 1/ 2012 , Volume 9 , pages: 2 , PubMed ID: 22300422
  • UNICAMP - IMECC - DMA, Praça Sérgio Buarque de Holanda, Campinas, SP, Brazil. hyunyang@ime.unicamp.br
  • BACKGROUND: Cancer arises when within a single cell multiple malfunctions of control systems occur, which are, broadly, the system that promote cell growth and the system that protect against erratic growth. Additional systems within the cell must be corrupted so that a cancer cell, to form a mass of any real size, produces substances that promote the growth of new blood vessels. Multiple mutations are required before a normal cell can become a cancer cell by corruption of multiple growth-promoting systems. METHODS: We develop a simple mathematical model to describe the solid cancer growth dynamics inducing angiogenesis in the absence of cancer controlling mechanisms. RESULTS: The initial conditions supplied to the dynamical system consist of a perturbation in form of pulse: The origin of cancer cells from normal cells of an organ of human body. Thresholds of interacting parameters were obtained from the steady states analysis. The existence of two equilibrium points determine the strong dependency of dynamical trajectories on the initial conditions. The thresholds can be used to control cancer. CONCLUSIONS: Cancer can be settled in an organ if the following combination matches: better fitness of cancer cells, decrease in the efficiency of the repairing systems, increase in the capacity of sprouting from existing vascularization, and higher capacity of mounting up new vascularization. However, we show that cancer is rarely induced in organs (or tissues) displaying an efficient (numerically and functionally) reparative or regenerative mechanism.
Contributors
Submitter of the first revision: Jinghao Men
Submitter of this revision: Jinghao Men
Modellers: Jinghao Men

Metadata information

is (2 statements)
BioModels Database MODEL1908140001
BioModels Database BIOMD0000000796

isDescribedBy (1 statement)
PubMed 22300422

hasTaxon (1 statement)
Taxonomy Homo sapiens

hasProperty (2 statements)
Mathematical Modelling Ontology Ordinary differential equation model
NCIt Tumor Angiogenesis


Curation status
Curated


Tags

Connected external resources

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Name Description Size Actions

Model files

Yang2012.xml SBML L3V1 representation of tumour angiogenesis model 90.47 KB Preview | Download

Additional files

Yang2012.cps CPS file of the model in COPASI 101.09 KB Preview | Download
Yang2012.sedml Auto-generated SEDML file 3.86 KB Preview | Download

  • Model originally submitted by : Jinghao Men
  • Submitted: Aug 14, 2019 4:33:47 PM
  • Last Modified: Aug 14, 2019 4:33:47 PM
Revisions
  • Version: 3 public model Download this version
    • Submitted on: Aug 14, 2019 4:33:47 PM
    • Submitted by: Jinghao Men
    • With comment: Automatically added model identifier BIOMD0000000796
Legends
: Variable used inside SBML models


Species
Species Initial Concentration/Amount
P

cell
0.0 mmol
A

cell
0.0 mmol
E

endothelial cell
10.0 mmol
C

cell
9.0 mmol
T

malignant cell
1.023 mmol
Reactions
Reactions Rate Parameters
P => A tme*d*P d = 0.1 1/d
=> A; T tme*e*T*A*(1-A/k4) k4 = 1.0 1; e = 0.01 1/d
E => P; T tme*y*T*E y = 0.01 1/d
=> E tme*a2*E*(1-E/k2) k2 = 20.0 1; a2 = 0.1 1/d
A => tme*u5*A u5 = 0.01 1/d
C => tme*u1*C u1 = 0.01 1/d
T => ; C tme*b2*C*T b2 = 0.01 1/d
C => ; T tme*b1*T*C b1 = 0.01 1/d
P => tme*u4*P u4 = 0.01 1/d
Curator's comment:
(added: 14 Aug 2019, 16:33:41, updated: 14 Aug 2019, 16:33:41)
Publication figure 1 reproduced as per literature. Figure data is generated using COPASI 4.26 (build 213).