Explain how the cell cycle is regulated to prevent uncontrolled cell division, with reference to cyclins and tumour suppressor genes.

Cyclins are synthesised during the cell cycle and reach a peak just before the cell enters the next phase; they are then targeted for degradation by the anaphase‑promoting complex. This regulated synthesis and degradation ensures that cyclin‑dependent kinases (CDKs) are only active at the correct time, allowing the cell to pass the G1, G2 and spindle‑assembly checkpoints.

Cyclins bind to CDKs, forming a complex that phosphorylates specific substrates. The phosphorylation events trigger the biochemical changes required for DNA replication, chromosome condensation, and mitotic spindle formation, thereby driving the cell cycle forward.

Tumour‑suppressor genes such as p53 and Rb encode proteins that act as brakes on the cycle. p53 can arrest the cell at the G1/S or G2/M checkpoints and can trigger apoptosis if DNA damage is irreparable. Rb binds E2F transcription factors; when hypophosphorylated it blocks E2F activity, preventing S‑phase entry.

If a loss‑of‑function mutation occurs in a tumour‑suppressor gene, these inhibitory controls are lost. The cell cycle proceeds unchecked, DNA damage is not repaired, and the cell can divide uncontrollably, leading to tumour formation.