D2.1.16 (HL)—Mutations in cell cycle genes

Mutations in cell-cycle control genes can activate oncogenes or disable suppressors, causing uncontrolled mitosis and tumour formation in tissues repeatedly.

Exam analysis

Chance of appearing4%of analysed past papers

Latest appearanceMay 2025

Most common paperPaper2

Typical marks1–4

Common command terms

State
Outline
Explain
Predict

Scoring notes

Common mistake: Describing cancer as ordinary growth without linking it to uncontrolled cell division.

Recent exam appearances

May 2025Paper1A ["HL"] · TZ319[ 1 ]D2.1.16 (HL)—Mutations in cell cycle genes

May 2023Paper2 ["HL"] · TZ26(a)[ 4 ]D2.1.16 (HL)—Mutations in cell cycle genes

May 2019Paper1 ["HL"] · TZ23[ 1 ]D2.1.16 (HL)—Mutations in cell cycle genes

May 2019Paper2 ["HL"] · TZ22(a)(ii)[ 2 ]D2.1.16 (HL)—Mutations in cell cycle genes

Coverage 2019–2025 · Updated 16 Jul 2026

Gene class	Normal role	Cancer-promoting change	Analogy
proto-oncogene	stimulates division when an appropriate signal is present	gain-of-function mutation creates an oncogene with excessive or constant activity	accelerator stuck on
tumour-suppressor gene	stops the cycle, repairs damage or promotes apoptosis	loss-of-function mutation removes restraint	brake lost

A mutant Ras oncogene can keep growth-signalling pathways active without the normal extracellular signal. One activated allele may be sufficient to increase signalling.

Loss of p53 function can prevent arrest or apoptosis after DNA damage. Because a remaining functional copy can still supply p53, both copies often need to be lost in the affected cell lineage.

Cancer usually develops through accumulated mutations and clonal selection, not one mutation that instantly creates a fully malignant tumour.

Property	Benign tumour	Malignant tumour
local growth	often slower and bounded	often faster and poorly controlled
invasion	does not invade neighbouring tissue	penetrates and damages neighbouring tissue
metastasis	absent	cells may detach, travel and form secondary tumours

Metastasis requires several steps: cells detach from the primary tumour, enter blood or lymph, survive transport, leave the vessel and establish a secondary tumour elsewhere.

A tumour is an abnormal mass produced by excess cell division. Not every tumour is cancerous; malignant invasion and metastatic capacity define cancerous behaviour.

A local benign tumour is contrasted with a malignant tumour invading neighbouring tissue and with cells spreading through a vessel to form a secondary tumour.

Growth or repair signal → G1 growth → S-phase genome replication → G2 preparation and checkpoint control → cyclin–CDK activation → mitosis and cytokinesis → daughter cells differentiate, replace tissue or re-enter the cycle

Oncogene activation can increase positive growth signalling, while tumour-suppressor loss can remove arrest, repair or apoptosis. Accumulated changes allow an abnormal clone to proliferate.

Evidence scale	Question it answers
cell-cycle proteins and genes	why is checkpoint control altered?
mitotic index	what fraction of sampled cells is dividing now?
tissue boundary	is the tumour local or invading?
secondary growths	has metastatic spread occurred?

Rapid division alone is not the whole definition of malignancy. A strong explanation connects molecular control failure to clonal growth, tissue invasion and possible metastasis.

[ 4 ]

Explain how changes to the cell cycle can result in tumour formation.

Concept essentials

Tumours result from uncontrolled cell division.
Oncogene mutations can disrupt cell-cycle regulation.
Loss of tumour suppressor function can remove checkpoint control.
A high mitotic index can indicate rapid tumour growth.