Cell cycle control and cancer
CIE A-Level BiologyΒ· 15 min read
1. Cell Cycle Checkpointsβ β ββββ± 4 min
Cell cycle checkpoint
A control point in the cell cycle where regulatory signals confirm conditions are suitable before the cell progresses to the next phase, preventing transmission of damaged DNA to daughter cells.
Example:
The G1 checkpoint checks for undamaged DNA before the cell enters S phase for DNA replication.
Three key checkpoints act as regulatory nodes to ensure accurate cell division. Each checkpoint stops the cell cycle if errors are detected, allowing time for repair or triggering programmed cell death if damage cannot be fixed.
G1 Checkpoint (Restriction Point): Occurs at the end of G1. Checks cell size, nutrient availability, growth signals, and undamaged DNA. Cells that do not pass enter the quiescent Gβ phase.
G2 Checkpoint: Occurs at the end of G2 before mitosis. Checks that all DNA is fully and correctly replicated, and that any damage is repaired.
Metaphase (Spindle Assembly) Checkpoint: Occurs at metaphase of mitosis. Checks that all sister chromatids are correctly attached to spindle microtubules from opposite poles.
Describe what happens if a cell with damaged DNA progresses past the G2 checkpoint.
- 1
Recall that the core function of the G2 checkpoint is to block entry into mitosis if DNA is damaged or incompletely replicated.
- 2
If damaged DNA passes the checkpoint, the cell will complete mitosis and divide, passing the damaged DNA (with its mutation) to both daughter cells.
- 3
If the mutation occurs in a gene that regulates cell division, it removes normal control mechanisms, leading to uncontrolled cell division and tumour formation.
2. Oncogenes and Tumour Suppressor Genesβ β β βββ± 5 min
Two main classes of genes regulate cell division, and mutations in these genes are the root cause of cancer development. Both classes work together to balance cell growth and division.
Oncogene
A mutated form of a normal proto-oncogene. Proto-oncogenes code for proteins that stimulate cell division in response to growth signals. A gain-of-function mutation creates an oncogene that produces an overactive protein, driving constant uncontrolled cell division even without growth signals.
Tumour suppressor gene
A gene that codes for proteins that inhibit cell division, repair damaged DNA, or trigger apoptosis (programmed cell death) when damage is detected. Loss-of-function mutations remove this inhibitory control, allowing uncontrolled division.
Explain why one mutated allele is enough to cause cancer via an oncogene, but not via a tumour suppressor gene.
- 1
Oncogenes are caused by dominant gain-of-function mutations. A single mutated allele produces enough overactive stimulatory protein to constantly drive cell division, so one mutation is sufficient.
- 2
Tumour suppressor genes require loss-of-function mutations. One functional, unmutated allele still produces enough inhibitory protein to slow cell division, so control is retained.
- 3
Only when both copies of the tumour suppressor gene are inactivated by mutation is all inhibitory control lost, leading to uncontrolled division.
3. Benign and Malignant Tumoursβ β ββββ± 3 min
Uncontrolled cell division produces an abnormal mass of cells called a tumour. Tumours are classified as either benign or malignant based on their growth, invasiveness, and ability to spread.
Feature | Benign Tumour | Malignant Tumour |
|---|---|---|
Growth rate | Slow | Rapid |
Invasion | Non-invasive, encapsulated | Invasive, no capsule |
Metastasis | No spread to other sites | Spreads via blood/lymph |
Health impact | Rarely life-threatening | Often life-threatening |
Cancer classification | Non-cancerous | Cancerous |
Why is metastasis dangerous for a patient?
- 1
Metastasis occurs when malignant cells break off from the primary tumour, travel through blood or lymph, and form new secondary tumours in distant organs.
- 2
Secondary tumours can form in multiple different organs across the body, so surgical removal of all cancerous tissue is usually not possible.
- 3
Metastatic cancer disrupts normal organ function in multiple sites, making treatment much less effective than for early, localised primary tumours.
4. Development of Cancerβ β β βββ± 3 min
Cancer is a multi-step disease that requires multiple independent mutations to accumulate in a single lineage of cells over time. Most cancers require 4-6 mutations in different regulatory genes before a tumour becomes malignant.
Explain why the incidence of cancer increases with age.
- 1
Cancer development requires multiple sequential mutations in cell cycle regulatory genes in a single cell lineage.
- 2
Random mutations accumulate over a person's lifetime, from both errors during DNA replication and ongoing exposure to environmental mutagens.
- 3
Older individuals have had more time to accumulate the required number of mutations, so the probability of developing cancer increases significantly with age.
5. Common Pitfalls
Wrong move:
Claiming one mutation in a tumour suppressor gene is enough to cause cancer
Why:
Tumour suppressor genes require loss-of-function mutations in both copies to remove all inhibitory control of division
Correct move:
State that both copies of a tumour suppressor gene must be inactivated to cause cancer, while one mutation in a proto-oncogene is enough to form a cancer-causing oncogene
Wrong move:
Referring to all tumours as cancer
Why:
Only malignant tumours are classified as cancer; benign tumours are non-invasive and non-cancerous
Correct move:
Use the term cancer only when describing malignant tumours, and clarify that benign tumours are non-cancerous growths
Wrong move:
Stating all checkpoints only check for DNA damage
Why:
Each checkpoint has a unique primary function beyond just checking for DNA damage
Correct move:
Specify each checkpoint's role: G1 checks growth signals/cell size, G2 checks complete replication, metaphase checks spindle attachment
Wrong move:
Claiming all mutations cause cancer
Why:
Most mutations do not affect genes that regulate cell division, so do not lead to cancer
Correct move:
Explain that cancer only develops when mutations accumulate in genes that control cell cycle progression and division
6. Quick Reference Cheatsheet
Component | Key Feature |
|---|---|
G1 Checkpoint | Checks DNA damage, nutrients, growth factors |
G2 Checkpoint | Checks complete DNA replication, no damage |
Metaphase Checkpoint | Checks all chromatids attached to spindle |
Proto-oncogene | Normal: stimulates cell division |
Oncogene | Mutated: overactive, drives uncontrolled division |
Tumour suppressor gene | Normal: inhibits division, needs 2 mutations to inactivate |
Benign tumour | Slow, non-invasive, no metastasis, non-cancerous |
Malignant tumour | Rapid, invasive, metastasis, cancerous |
7. Frequently Asked
Do I need to know specific named genes (like p53) for the exam?
No, CIE 9700 only requires you to understand the general roles of oncogenes and tumour suppressor genes; named examples are not required for marks.
When this came up on past exams
AI-estimated based on syllabus patterns β cross-check with official past papers for accuracy. Use only as revision-focus signals.
- 2022 Β· 22
Compare benign and malignant tumours
- 2021 Β· 11
Role of cell cycle checkpoints
- 2023 Β· 21
Oncogenes vs tumour suppressor genes
Going deeper
What's Next
Understanding cell cycle control and cancer forms the foundation for many other topics in CIE A-Level Biology. The concepts of mutation and uncontrolled growth connect directly to meiosis, where errors in cell division lead to chromosome abnormalities and genetic disorders. This topic also underpins later study of cancer biology and treatments, which often appear in extended response questions. Mastery of the core distinctions between oncogenes and tumour suppressor genes, and benign vs malignant tumours, is critical as this sub-topic is regularly assessed in both multiple choice and structured paper 2 questions.