Simulating the Hallmarks of cancer

Robert G. Abbott, Stephanie Forrest, Kenneth Pienta

Research output: Contribution to journalArticle

Abstract

Cancer can be viewed as the loss of cooperative cell behaviors that normally facilitate multicellularity, including the formation of tissues and organs. Hanahan and Weinberg describe the phenotypic differences between healthy and cancerous cells in an article titled "Me Hallmarks of Cancer" (Cell, 100, 57-70, 2000). Here the authors propose six phenotypic changes at the cellular level as the essential hallmarks of cancer. They investigate the dynamics and interactions of these hallmarks in a model known as CancerSim. They describe how CancerSim implements the hallmarks in an agent-based simulation which can help test the hypotheses put forth by Hanahan and Weinberg. Experiments with CancerSim are described that study the interactions of cell phenotype alterations, and in particular, the likely sequences of precancerous mutations, known as pathways. The experiments show that sequencing is an important factor in tumorigenesis, as some mutations have preconditions - they are selectively advantageous only in combination with other mutations. CancerSim enables a modeler to study the dynamics of a developing tumor and simulate how progression can be altered by tuning model parameters.

Original languageEnglish (US)
Pages (from-to)617-634
Number of pages18
JournalArtificial Life
Volume12
Issue number4
DOIs
StatePublished - Sep 2006
Externally publishedYes

Fingerprint

Cancer
Mutation
Cell
Tumors
Neoplasms
Tuning
Experiments
Tissue
Agent-based Simulation
Precondition
Progression
Interaction
Phenotype
Cell Communication
Sequencing
Cooperative Behavior
Experiment
Tumor
Pathway
Carcinogenesis

Keywords

  • Agent simulation
  • Cancer
  • Cellular automata

ASJC Scopus subject areas

  • Control and Systems Engineering
  • Artificial Intelligence
  • Theoretical Computer Science
  • Computational Theory and Mathematics

Cite this

Simulating the Hallmarks of cancer. / Abbott, Robert G.; Forrest, Stephanie; Pienta, Kenneth.

In: Artificial Life, Vol. 12, No. 4, 09.2006, p. 617-634.

Research output: Contribution to journalArticle

Abbott, Robert G. ; Forrest, Stephanie ; Pienta, Kenneth. / Simulating the Hallmarks of cancer. In: Artificial Life. 2006 ; Vol. 12, No. 4. pp. 617-634.
@article{239b2e7ab09243839d7fe7291382718c,
title = "Simulating the Hallmarks of cancer",
abstract = "Cancer can be viewed as the loss of cooperative cell behaviors that normally facilitate multicellularity, including the formation of tissues and organs. Hanahan and Weinberg describe the phenotypic differences between healthy and cancerous cells in an article titled {"}Me Hallmarks of Cancer{"} (Cell, 100, 57-70, 2000). Here the authors propose six phenotypic changes at the cellular level as the essential hallmarks of cancer. They investigate the dynamics and interactions of these hallmarks in a model known as CancerSim. They describe how CancerSim implements the hallmarks in an agent-based simulation which can help test the hypotheses put forth by Hanahan and Weinberg. Experiments with CancerSim are described that study the interactions of cell phenotype alterations, and in particular, the likely sequences of precancerous mutations, known as pathways. The experiments show that sequencing is an important factor in tumorigenesis, as some mutations have preconditions - they are selectively advantageous only in combination with other mutations. CancerSim enables a modeler to study the dynamics of a developing tumor and simulate how progression can be altered by tuning model parameters.",
keywords = "Agent simulation, Cancer, Cellular automata",
author = "Abbott, {Robert G.} and Stephanie Forrest and Kenneth Pienta",
year = "2006",
month = "9",
doi = "10.1162/artl.2006.12.4.617",
language = "English (US)",
volume = "12",
pages = "617--634",
journal = "Artificial Life",
issn = "1064-5462",
publisher = "MIT Press Journals",
number = "4",

}

TY - JOUR

T1 - Simulating the Hallmarks of cancer

AU - Abbott, Robert G.

AU - Forrest, Stephanie

AU - Pienta, Kenneth

PY - 2006/9

Y1 - 2006/9

N2 - Cancer can be viewed as the loss of cooperative cell behaviors that normally facilitate multicellularity, including the formation of tissues and organs. Hanahan and Weinberg describe the phenotypic differences between healthy and cancerous cells in an article titled "Me Hallmarks of Cancer" (Cell, 100, 57-70, 2000). Here the authors propose six phenotypic changes at the cellular level as the essential hallmarks of cancer. They investigate the dynamics and interactions of these hallmarks in a model known as CancerSim. They describe how CancerSim implements the hallmarks in an agent-based simulation which can help test the hypotheses put forth by Hanahan and Weinberg. Experiments with CancerSim are described that study the interactions of cell phenotype alterations, and in particular, the likely sequences of precancerous mutations, known as pathways. The experiments show that sequencing is an important factor in tumorigenesis, as some mutations have preconditions - they are selectively advantageous only in combination with other mutations. CancerSim enables a modeler to study the dynamics of a developing tumor and simulate how progression can be altered by tuning model parameters.

AB - Cancer can be viewed as the loss of cooperative cell behaviors that normally facilitate multicellularity, including the formation of tissues and organs. Hanahan and Weinberg describe the phenotypic differences between healthy and cancerous cells in an article titled "Me Hallmarks of Cancer" (Cell, 100, 57-70, 2000). Here the authors propose six phenotypic changes at the cellular level as the essential hallmarks of cancer. They investigate the dynamics and interactions of these hallmarks in a model known as CancerSim. They describe how CancerSim implements the hallmarks in an agent-based simulation which can help test the hypotheses put forth by Hanahan and Weinberg. Experiments with CancerSim are described that study the interactions of cell phenotype alterations, and in particular, the likely sequences of precancerous mutations, known as pathways. The experiments show that sequencing is an important factor in tumorigenesis, as some mutations have preconditions - they are selectively advantageous only in combination with other mutations. CancerSim enables a modeler to study the dynamics of a developing tumor and simulate how progression can be altered by tuning model parameters.

KW - Agent simulation

KW - Cancer

KW - Cellular automata

UR - http://www.scopus.com/inward/record.url?scp=33748509962&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748509962&partnerID=8YFLogxK

U2 - 10.1162/artl.2006.12.4.617

DO - 10.1162/artl.2006.12.4.617

M3 - Article

VL - 12

SP - 617

EP - 634

JO - Artificial Life

JF - Artificial Life

SN - 1064-5462

IS - 4

ER -