Cancer Genetics Simulator

Cancer arises from an accumulation of somatic mutations, not a single event. This simulator models a growing clonal population starting from one normal cell on a 3D lattice: at every step each cell may divide into a free neighboring slot or undergo apoptosis, with both probabilities set by which driver mutations it carries. Oncogenes like RAS and MYC raise the division rate when activated; tumor-suppressor genes like TP53 and RB normally trigger apoptosis in damaged cells, so losing one lets damage go unpunished. Microsatellite instability controls how fast new drivers appear at each division. Tune the sliders to see how a tissue tips from stable turnover into unchecked clonal expansion — and watch which color, the malignant red double-mutants, ends up dominating the mass.