Biology
The cell cycle & how cancer goes wrong — quick study summary
The cell cycle has four phases: G1 (growth), S (DNA synthesis), G2 (growth + check), and M (mitosis). Checkpoints at G1/S, G2/M, and during M ensure damaged DNA is repaired or the cell is destroyed by apoptosis before dividing. Cancer arises when mutations disable these checkpoints — usually in tumour suppressor genes (e.g. p53) or proto-oncogenes (e.g. Ras). Unchecked division produces a tumour; metastasis is when cancer cells spread through blood or lymph.
Key points
- G1 → S → G2 → M; checkpoints at G1/S, G2/M, and during mitosis
- p53 ('guardian of the genome') triggers repair or apoptosis on DNA damage
- Proto-oncogenes (Ras, Myc) become oncogenes when over-active
- Cancer = uncontrolled division + evasion of apoptosis + (often) metastasis
- Tumour suppressor loss is recessive at the cell level: BOTH copies must fail
Practice quiz
Click each question to reveal the answer.
1. Which protein is known as the 'guardian of the genome'?
- Cyclin
- p53
- Ras
- Myc
Answer: p53
p53 detects DNA damage and triggers repair or apoptosis. Mutated p53 is found in ~50% of human cancers.
2. What's the difference between a proto-oncogene and an oncogene?
Answer: A proto-oncogene is the normal, regulated version; an oncogene is the over-active mutated version that drives cancer
Proto-oncogenes normally drive controlled growth. A gain-of-function mutation turns them into oncogenes that drive uncontrolled division.
3. What is metastasis?
Answer: Cancer cells spreading from the original tumour to other parts of the body
Metastatic cancer is the major cause of cancer death — it spreads via blood and lymph to seed secondary tumours.
Last reviewed: May 2026