Bioengineering, Food, and Natural Products

Modeling the effect of chemotaxis on glioblastoma tumor progression

  1. Francisco G. Vital-Lopez1,
  2. Antonios Armaou1,
  3. Michelle Hutnik2,
  4. Costas D. Maranas1,*

Article first published online: 14 MAY 2010

DOI: 10.1002/aic.12296

Issue

AIChE Journal

AIChE Journal

Volume 57, Issue 3, pages 778–792, March 2011

Additional Information

How to Cite

Vital-Lopez, F. G., Armaou, A., Hutnik, M. and Maranas, C. D. (2011), Modeling the effect of chemotaxis on glioblastoma tumor progression. AIChE J., 57: 778–792. doi: 10.1002/aic.12296

Author Information

  1. 1

    Dept. of Chemical Engineering, The Pennsylvania State University, University Park, PA 16802

  2. 2

    Medical Science Dept., The Angiogenesis Foundation, Cambridge, MA 02238

*Dept. of Chemical Engineering, The Pennsylvania State University, University Park, PA 16802

Publication History

  1. Issue published online: 14 MAY 2010
  2. Article first published online: 14 MAY 2010
  3. Accepted manuscript online: 14 MAY 2010 12:00AM EST
  4. Manuscript Revised: 17 APR 2010
  5. Manuscript Received: 1 JAN 2010

Funded by

  • Penn State Institute for CyberScience Seed Funding
  • National Science Foundation (NSF-CAREER award). Grant Number: CBET 06-44519

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Keywords:

  • glioblastoma;
  • modeling of tumor dynamics;
  • signaling in tumor growth;
  • 3-D tumor morphology

Abstract

Tumor progression depends on the intricate interplay between biological processes that span the molecular and macroscopic scales. A mathematical agent-based model is presented to describe the 3-D (three-dimensional) progression of a brain tumor type (i.e., glioblastoma multiforme) as the collective behavior of individual tumor cells whose fate is determined by intracellular signaling pathways (i.e., MAPK pathway) that are governed by the temporal-spatial distribution of key biochemical cues (i.e., growth factors, nutrients). The model is used to investigate how tumor growth and invasiveness depend on the response of migrating tumor cells to chemoattractants. Simulation results suggest that individual cell sensitivity to chemical gradients is necessary to generate in silico tumors with the irregular shape and diffusive tumor-stroma interface characteristic of glioblastomas. In addition, vascular network damage influences tumor growth and invasiveness. The results quantitatively recapitulate the central role that nutrient availability and signaling proteins have on tumor invasive properties. © 2010 American Institute of Chemical Engineers AIChE J, 2011

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