Hallmark Toggles
① Sustained Growth Signals
Cancer cells produce their own mitogenic signals. Division rate ↑ 6×; cells expand perpendicular to the epithelial line (hyperplasia).
② Evade Growth Suppression
Loss of contact inhibition (RB/p27 loss). Cancer cells ignore crowding signals and continue dividing even when packed with neighbors.
③ Resist Apoptosis
p53 loss or BCL2 upregulation. Cancer cells no longer die stochastically — cell death rate drops to ~0. Cells accumulate indefinitely.
④ Replicative Immortality
Telomerase reactivation. Normal cells have a Hayflick limit (~50 divisions). Cancer cells remove this cap — unlimited proliferation potential.
⑤ Induce Angiogenesis
VEGF secretion recruits new blood vessels. Without this, inner tumor cells die from hypoxia. With it, the tumor can grow beyond ~2mm.
⑥ Invasion & Metastasis
E-cadherin loss + EMT. Rare cancer cells stochastically undergo EMT and migrate freely through tissue — long-range spread beyond the primary site.
Live Statistics
Normal cells
60
Cancer cells
1
Hyperplasia ht
1
Time (steps)
0
Max divisions
0
Migrant cells
0
Ready — press Run to start the simulation.
Epithelial Tissue View
Normal epithelial cell
Cancer cell (primary)
Dead / apoptotic
Vessel (angiogenesis)
Migrant cancer cell
← Position along epithelial line · Y-axis = perpendicular (hyperplasia) →
Current Run — Snapshots (every 200 steps)
Snapshots will appear here as the simulation runs.
Cell Populations
Hyperplasia Height
Cancer Fraction
Simulation History — newest run at top · snapshots every 200 steps
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