Cell division is controlled by genes, and genes can mutate — including the genes that do the controlling. When that happens, a cell stops listening to the signals telling it when to stop. Cancer is what a broken cell cycle looks like from the outside.
📘 What you need to know
Mutations in the genes that control the cell cycle can lead to cancer. Two types of gene are involved.
Proto-oncogenes code for proteins that stimulate normal cell division. When mutated they become oncogenes, producing more protein or permanently activated protein.
Tumour-suppressor genes code for proteins that inhibit cell division or trigger apoptosis (controlled cell death) when DNA is damaged. Mutations give less protein, no protein, or permanently deactivated protein.
Either way the result is uncontrolled mitosis, producing an irregular mass of cells called a tumour.
Malignant tumours are cancerous: they grow rapidly, invade and destroy surrounding tissue, and can metastasise to form secondary tumours.
Benign tumours are non-cancerous: they grow slowly, do not invade or metastasise, and usually do not return after removal.
Malignant tumours can be initiated by carcinogens such as UV or X-ray exposure, tobacco, asbestos and processed meat.
Two genes, two ways to lose control
You met oncogenes briefly on Consequences of Mutations. Here is the full picture, and the key is that there are two opposite failures that produce the same outcome.
Proto-oncogenes: the accelerator
These genes normally code for proteins that stimulate cell division — a healthy, necessary job. A mutation converts a proto-oncogene into an oncogene. The result is either an increase in the amount of protein produced, or a protein that is permanently activated. Division is being pushed on constantly.
Tumour-suppressor genes: the brake
These code for proteins that inhibit cell division, or that promote apoptosis if the nucleus contains damaged DNA. A mutation may mean no protein, reduced protein, or protein that is permanently deactivated. The brake has failed.
This is why cancers usually need several mutations. One faulty control gene is often not enough on its own.
The car analogy is worth keeping, but hold it loosely. The real point is the direction of the change: an oncogene produces too much or too active a protein, while a tumour-suppressor mutation produces too little or inactive protein. Examiners want that contrast stated.
What a tumour is
Cancerous cells divide repeatedly and uncontrollably by mitosis, forming a tumour: an irregular mass of cells. By the time a typical tumour is detected it contains around a thousand million cells.
All tumours, cancerous or not, can harm the body by:
damaging the organ in which they are growing;
causing blockages or obstructions;
exerting pressure on other organs.
Malignant and benign
Feature
Malignant (cancerous)
Benign (non-cancerous)
Growth rate
Rapid
Slow
Effect on neighbouring tissue
Invades and destroys it
Does not invade
Spread to other organs
Yes — metastasis
No — does not metastasise
After surgical removal
Secondary tumours can still grow back
Usually does not return
Typical causes
Carcinogens such as UV, X-rays, tobacco, asbestos, processed meat
Inflammation or infection, injury, diet, genetics, toxins and radiation
Metastasis
A malignant tumour grows rapidly and then invades and destroys surrounding tissue. Cells within it secrete chemicals that cause blood vessels to form, supplying the tumour with nutrients, growth factors and oxygen. This original tumour is the primary tumour.
Cells can then break off and travel through the bloodstream or lymphatic system to other parts of the body. That spread is metastasis, and the tumours that develop from those escaped cells are secondary tumours. This is why cancer can affect multiple organs, and why it can return after surgery.
Examples of benign tumours include polyps in the nose, colon and ovaries, non-cancerous brain tumours, and warts caused by a viral infection.
A benign tumour can still be dangerous — pressure on a vital organ is serious — but it stays where it started.
Worked examples
WORKED EXAMPLE
Classifying a gene
A gene codes for a protein that triggers apoptosis when DNA damage is detected. A mutation means no functional protein is made. Name this type of gene and explain the consequence.
Step 1: Identify the normal role
Promoting apoptosis in damaged cells is an inhibitory role, so this is a tumour-suppressor gene.
Step 2: State what the mutation removes
Without functional protein, damaged cells are no longer destroyed.
Step 3: Follow the consequence
Cells with damaged DNA survive and continue dividing, so mutations accumulate and uncontrolled mitosis may follow.
A tumour-suppressor gene; damaged cells survive and keep dividingAsk yourself whether the normal protein pushes division on or holds it back.
WORKED EXAMPLE
Why cancer returns after surgery
A malignant primary tumour is removed surgically, but tumours later appear in the patient’s liver and lungs. Explain this observation.
Step 1: Name the processMetastasis — cells broke away from the primary tumour before it was removed.
Step 2: State the route
They travelled through the bloodstream or lymphatic system.
Step 3: Explain the new tumours
Those cells settled in other organs and divided by uncontrolled mitosis, forming secondary tumours.
Cells had already metastasised before the primary tumour was removedSay primary and secondary explicitly — both terms usually carry marks.
WORKED EXAMPLE
Comparing two tumours
Two patients each have a tumour. One is benign, the other malignant. State two differences in the behaviour of the tumours.
Difference 1: rate of growth
The malignant tumour grows rapidly; the benign one grows slowly.
Difference 2: spread
The malignant tumour invades surrounding tissue and metastasises; the benign one stays where it is.
A useful third point
A benign tumour usually does not return after removal; a malignant one can.
Growth rate, and the capacity to invade and metastasiseBoth tumours can still cause harm by pressure or blockage — do not say benign means harmless.
💡 Exam tip
Contrast the two gene types by direction: oncogenes give too much or over-active protein; tumour-suppressor mutations give too little or inactive protein.
Use the term proto-oncogene for the healthy version and oncogene only for the mutated one.
Include apoptosis when describing tumour-suppressor genes.
The two differences examiners look for are rate of division and growth, and capacity for metastasis and invasion.
Name specific carcinogens rather than saying “harmful substances”.
Remember benign tumours can still damage the body by pressure and blockage.
⚠ Common mix-up
Saying benign tumours are harmless. They can obstruct or press on organs.
Calling every mutated gene an oncogene. It specifically means a mutated proto-oncogene that causes cancer.
Mixing up the two gene types. One stimulates division, the other inhibits it.
Thinking a tumour is the same as metastasis. The tumour is the mass; metastasis is the spread.
Saying cancer is caused by one mutation. Several control genes usually have to fail.
Confusing carcinogen and oncogene. A carcinogen is an external agent; an oncogene is a mutated gene.
Up next: Mitotic Index (Skills) — a way to measure how fast a tissue is dividing. It is used in cancer diagnosis for exactly the reasons on this page, and it is one of the easiest calculations in the course.
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