A resource-based mechanistic framework for castration-resistant prostate cancer (CRPC).

Cancer therapy often leads to the selective elimination of drug-sensitive cells from the tumour. This can favour the growth of cells resistant to the therapeutic agent, ultimately causing a tumour relapse. Castration-resistant prostate cancer (CRPC) is a well-characterised instance of this phenomenon.

Context-dependent selection as the keystone in the somatic evolution of cancer.

Somatic evolution of cancer involves a series of mutations, and attendant changes, in one or more clones of cells. A "bad luck" type model assumes chance accumulation of mutations. The clonal expansion model assumes, on the other hand, that any mutation leading to partial loss of regulation of cell proliferation will give a selective advantage to the mutant.

Inferring causal pathways among three or more variables from steady-state correlations in a homeostatic system.

Cross-sectional correlations between two variables have limited implications for causality. We examine here whether it is possible to make causal inferences from steady-state data in a homeostatic system with three or more inter-correlated variables. Every putative pathway between three variables makes a set of differential predictions that can be tested with steady state data.