Hermann B. Frieboes

TL;DR: In this paper, the authors provide an overview of multiscale modelling focusing on the growth phase of tumours and bypassing the initial stage of tumourigenesis, and limit the scope further by considering models of tumor progression that do not distinguish tumour cells by their age and do not consider immune system interactions nor do they describe models of therapy.

TL;DR: This is the first paper in a two-part series in which a diffuse interface continuum model of multispecies tumor growth and tumor-induced angiogenesis in two and three dimensions is developed, analyzed, and simulated.

TL;DR: It is proposed that tumor morphogenesis in vivo may be a function of marginally stable environmental conditions caused by spatial variations in cell nutrients, oxygen, and growth factors, and that controlling these conditions by decreasing spatial gradients could benefit treatment outcomes, whereas current treatment, and especially antiangiogenic therapy, may trigger spatial heterogeneity, thus causing invasive instability.

TL;DR: This model enables correlation of glioma morphology to tumor growth by quantifying interdependence of tumor mass on the microenvironment and on the cellular phenotypes, and can be used for disease diagnosis/prognosis, hypothesis testing, and to guide surgery and therapy.

TL;DR: Heterogeneity in the physiologically complex tumor microenvironment, caused by non-uniform distribution of oxygen, cell nutrients, and metabolites, as well as phenotypic changes affecting cellular-scale parameters, can be quantitatively linked to the tumor macro-scale as a mechanism that promotes morphological instability.