Density-dependent quiescence in glioma invasion: instability in a simple reaction–diffusion model for the migration/proliferation dichotomy
Type
ArticleAuthors
Pham, KaraChauviere, Arnaud
Hatzikirou, Haralambos
Li, Xiangrong
Byrne, Helen M.

Cristini, Vittorio
Lowengrub, John
KAUST Grant Number
KUK-C1-013-04Date
2012-01Permanent link to this record
http://hdl.handle.net/10754/597928
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Gliomas are very aggressive brain tumours, in which tumour cells gain the ability to penetrate the surrounding normal tissue. The invasion mechanisms of this type of tumour remain to be elucidated. Our work is motivated by the migration/proliferation dichotomy (go-or-grow) hypothesis, i.e. the antagonistic migratory and proliferating cellular behaviours in a cell population, which may play a central role in these tumours. In this paper, we formulate a simple go-or-grow model to investigate the dynamics of a population of glioma cells for which the switch from a migratory to a proliferating phenotype (and vice versa) depends on the local cell density. The model consists of two reaction-diffusion equations describing cell migration, proliferation and a phenotypic switch. We use a combination of numerical and analytical techniques to characterize the development of spatio-temporal instabilities and travelling wave solutions generated by our model. We demonstrate that the density-dependent go-or-grow mechanism can produce complex dynamics similar to those associated with tumour heterogeneity and invasion.Citation
Pham K, Chauviere A, Hatzikirou H, Li X, Byrne HM, et al. (2012) Density-dependent quiescence in glioma invasion: instability in a simple reaction–diffusion model for the migration/proliferation dichotomy. Journal of Biological Dynamics 6: 54–71. Available: http://dx.doi.org/10.1080/17513758.2011.590610.Sponsors
J.L., K.P. and X.L. acknowledge support from the National Science Foundation Division of Mathematical Sciences (DMS) and from the National Institutes of Health through grant P50GM76516 for a Centre of Excellence in Systems Biology at the University of California, Irvine. A. C., H. H. and V. C. acknowledge support from The Cullen Trust for Health Care and the National Institute for Health, Integrative Cancer Biology Program: 1U54CA149196, for the Center for Systematic Modeling of Cancer Development. V. C. also acknowledges the National Science Foundation, Division of Mathematical Sciences for grant DMS-0818104. H. B. acknowledges partial support by Award No. KUK-C1-013-04, made by King Abdullah University of Science and Technology (KAUST).Publisher
Informa UK LimitedJournal
Journal of Biological DynamicsPubMed ID
22873675PubMed Central ID
PMC3623708ae974a485f413a2113503eed53cd6c53
10.1080/17513758.2011.590610
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