Tumor architecture and emergence of strong genetic alterations are bottlenecks for clonal evolution in primary prostate cancer.

Prostate cancer (PCA) exhibits high levels of intratumoral heterogeneity. In this study, we developed a mathematical model to study the growth and genetic evolution of PCA. We explored the possible evolutionary patterns and demonstrated that tumor architecture represents a major bottleneck for divergent clonal evolution.

Traveling waves of an FKPP-type model for self-organized growth.

We consider a reaction-diffusion system of densities of two types of particles, introduced by Hannezo et al. (Cell 171(1):242-255.e27, 2017).

Active bundles of polar and bipolar filaments.

Bundles of actin filaments and molecular motors of the myosin family are a common subcellular organizational motif. Typically, such bundles are under contractile stress resulting from interactions between the filaments and the motors. This holds in particular for contractile rings that appear in the late stages of cell division in animal cells and that cleave the mother into two daughter cells.