Cancer Genetics Simulator | mysimulator.uk

Cancer Genetics

Oncogene activation 0.30

Suppressor loss 0.30

MSI mutation rate 1.5×

Population

–

Malignant

–

Generation

–

Driver mutations

–

How it works

Each cell divides or dies every step according to two families of mutation. Oncogenes such as RAS and MYC act like a stuck gas pedal — activating one raises a cell's division probability. Tumor-suppressor genes such as TP53 and RB act like brakes that trigger apoptosis when DNA damage is detected — losing one lets a damaged cell keep dividing instead of dying. A cell that has acquired both is a fully transformed clone: fast division, near-immune to apoptosis. Microsatellite instability (MSI) is a broken DNA-repair proofreading system — it doesn't change either rate directly, it multiplies how often new driver mutations appear at each division, seeding more of both.

P(divide)    = 0.07 · (3.2 if onco) · (2.8 if supp) · (1.5 if both)
P(apoptosis) = 0.025 · (0.12 if supp) · (1.15 if onco&!supp)
P(new driver) = rate_slider · 0.03 · MSI×

Oncogene activation — chance a dividing cell's daughter gains a RAS/MYC-style driver, pushing the division rate up.
Suppressor loss — chance a daughter loses TP53/RB-style protection, collapsing its apoptosis rate.
MSI mutation rate — multiplies both mutation chances; a genomically unstable clone accumulates drivers far faster.
Colors — green cells are unmutated tissue, amber have only an active oncogene, purple have only lost a suppressor, red have both and are the malignant clone actually driving tumor growth.

Real-world relevance: this two-hit pattern — a gas-pedal mutation plus a lost brake — is why cancer is rarely caused by one mutation alone, and why liquid biopsies that sequence circulating tumor DNA look specifically for these driver combinations to flag malignancy early.

Normal cell Oncogene active Suppressor lost Malignant (both)

⚠ Couldn't load the 3D engineThree.js failed to load from the CDN. Check your connection and reload.