Review Article

In Silico Modelling of Tumour Margin Diffusion and Infiltration: Review of Current Status

Table 1

A summary of analytical models of tumour proliferation and diffusion.

TypeSite of modellingIncorporated mechanismsModel validation and resultsCommentsReference

ContinuumGliomaRandom motility with uniform diffusion; exponential proliferationN/APrediction of basic behaviour of gliomas (e.g., tumour cell density is a function of )Cruywagen et al. 1995 [14]
ContinuumAstrocytomaRandom motility with uniform diffusion; logistic proliferation; cell loss due to chemotherapy12 CT images of a patient/agreement between model parameters and experimental dataThe model is applicable for a specific course of treatmentTracqui et al. 1995 [12]
Mechano-chemicalMultisiteUniform diffusion; logistic proliferation; ECM-cell adhesion; haptotaxisN/AWhile important mechanisms in tumour invasion are considered, the behaviour of tumour at cellular level cannot be predictedTracqui 1995 [16]
ContinuumGliomaRandom motility with nonuniform diffusion; exponential proliferationVirtual MRI image/obtaining nonisotropic invasion patternRough prediction of the extent and concentration of local invasion. Applicable for tumours >1 (mm)3 Swanson et al. 2002, 2000 [2, 17]
ContinuumGlioblastomaNonuniform diffusion; exponential proliferation; mass effectMR images/capable to simulate complex tumour behaviourMigration and departure of cells not taken into accountClatz et al. 2005 [10]
Continuum-StochasticMultisiteRandom motility with uniform diffusion; haptotaxis; three-population tumour cells; heterogeneous ECMModel predictions consistent with clinical findings [18]Stochastic nature of the model allows to predict avascular invading tumour morphology by following individual cells with different phenotypes at each time and space stepAnderson 2005 [19]
ContinuumGliomaRandom motility with uniform diffusion; logistic proliferation; radially biased motility; shedding of invasive cell at tumour surfaceThe model reproduces in vitro experiments dataAssuming two-population tumour cells, proliferative (core) and invasive (periphery), and modelling invasive cells. Applicable for tumours <1 (mm)3Stein et al. 2007 [20]
ContinuumMultisiteRandom motility with uniform diffusion; logistic proliferation; ECM-cell adhesion; haptotaxis, Cell-cell adhesionComparison to simulation results of Anderson et al. [21]Simplifying assumptions: uniform diffusion and that haptotaxis is independent of ECM density; the simulation is 2DGerisch and Chaplain 2008 [6]
ContinuummultisiteRandom motility with uniform diffusion; logistic proliferation; two-population tumour cells; oxygen concentrationIn vivo tumour growth observationAssumption: cells could either proliferate or migrate where transition between these two classes is environment-dependent; haptotaxis not consideredThalhauser et al. 2009 [22]
Continuum-StochasticGliomaRandom motility with nonuniform diffusion; logistic proliferation; two-population tumour cells; haptotaxisThe model predicts the tumour growth pattern of a clinical caseStochastic step of the model allows for introduction of patient-specific parameters (e.g., tumour location)Eikenberry et al. 2009 [8]
ContinuumGliomaRandom motility with nonuniform diffusion; logistic proliferation; radiotherapyThe biopsies of nine patients/the model reproduces RT responseIn contrast with imaging-based RT response, this model incorporates patient-specific tumour growth kinetics to quantify RT outcomeRockne et al. 2010 [23]