Mutations in cell-cycle control genes can activate oncogenes or disable suppressors, causing uncontrolled mitosis and tumour formation in tissues repeatedly.
Coverage 2019–2025 · Updated 16 Jul 2026
Mutations can cause uncontrolled cell division by converting proto-oncogenes into oncogenes or by disabling tumour-suppressor genes.
| Gene class | Normal role | Cancer-promoting mutation |
|---|---|---|
| Proto-oncogene | Promotes division only when appropriate | Gain of function produces an oncogene that sends excessive growth signals |
| Tumour-suppressor gene | Slows the cycle, enforces checkpoints or prevents damaged cells dividing | Loss of function removes a brake on division |
A clone carrying one control mutation can continue dividing and acquire further mutations, progressively weakening the systems that restrain proliferation.
An activated oncogene can keep a growth pathway switched on while loss of a tumour suppressor allows damaged cells to pass a checkpoint; together they strongly favour tumour growth.
One mutation does not guarantee cancer. Several independent controls normally limit division, so tumour development often involves accumulated mutations.
This objective is assessed through structured response, commonly using State / Outline / Explain.
State / Outline / Explain / Predict
Build the answer around this relationship: Tumours result from uncontrolled cell division.
Describing cancer as ordinary growth without linking it to uncontrolled cell division.
Representative question
Explain how changes to the cell cycle can result in tumour formation.
Cell proliferation increases cell number by repeated mitosis, as in plant meristems, early embryos, skin replacement, and wound healing. The cell cycle includes interphase, mitosis, and cytokinesis; interphase has G1 growth, S-phase DNA replication, and G2 preparation. Interphase is metabolically active, not resting; cells synthesize proteins, replicate DNA, grow cytoplasm, and increase organelles. Cyclin concentrations rise and fall to activate cyclin-dependent kinases; CDK-cyclin complexes such as MPF control checkpoints and mitosis entry. Proto-oncogene activation and tumour suppressor loss disrupt checkpoints; accumulated mutations can cause uncontrolled proliferation and cancer. Benign tumours grow locally, malignant tumours invade neighbouring tissues, and metastasis spreads cancer cells to form secondary tumours.
