Fig. 4

Schematic showing clonal evolution in cancer and the possible role of p53 amyloid. According to the clonal dominance hypothesis, metastatic subclones inside the main tumour may outgrow and take control of the tumour bulk. According to the clonal selection model of metastasis, the subpopulations of cell populations that are capable of spreading are the ones that do so. As per the parallel evolution hypothesis, metastasis develops early in the course of a tumour and is not dependent on the presence of tumour cells in the primary site. Due to the various mutations, the subclones have different genotypes. We hypothesize that these mutations acquired by p53 gene results in amyloid formation with varied phenotypes leading to clonal evolution