Normal cell division and its control
Your body has about 30 trillion cells. New cells come from mitosis: one cell copies its DNA and splits into two identical cells. This happens only when needed, for growth, healing or replacing old cells (for example skin and blood cells).
The cell cycle has checkpoints, like traffic lights. The cell checks: Is my DNA undamaged? Is there space? Has the body sent a 'grow' signal? Normal cells also stop dividing when they touch their neighbours (contact inhibition) and can divide only a limited number of times.
Genes that control this:
- Proto-oncogenes: the accelerator. They tell a cell to divide when needed.
- Tumour-suppressor genes (for example p53): the brake. They stop division if something is wrong.
- DNA-repair genes: the mechanics. They fix copying mistakes.
- If damage cannot be fixed, the cell kills itself neatly: apoptosis (programmed cell death).
How cancer starts: mutations and uncontrolled division
A mutation is a change in the DNA code. Most mutations are repaired or harmless. Cancer begins when several mutations build up in one cell and hit the control genes:
- a proto-oncogene becomes an oncogene: accelerator stuck ON;
- a tumour-suppressor gene stops working: brake broken;
- repair and apoptosis fail, so the damaged cell survives.
Now the cell divides without control. Each round doubles the number: 1 → 2 → 4 → 8 … After 10 doublings there are 1024 cells; after 30 doublings about 1 billion, a lump about 1 cm across. This mass of extra cells is a tumour (or neoplasm). Because it usually takes many mutations, most cancers appear in older people.
Cancer cells also differ from normal cells: they ignore contact inhibition, can divide endlessly, often have odd shapes and big nuclei, and send signals that make new blood vessels grow to feed the tumour (angiogenesis).
Benign and malignant tumours, and metastasis
| Benign tumour | Malignant tumour (cancer) | |
|---|---|---|
| Growth | Slow | Often fast |
| Edges | Inside a capsule, clear border | No capsule, invades nearby tissue |
| Spread | Does not spread | Can spread (metastasis) |
| Danger | Usually not life-threatening, unless it presses on an organ such as the brain | Life-threatening if not treated |
| Example | Wart, lipoma (fatty lump) | Lung, breast, skin melanoma, leukaemia |
Metastasis: malignant cells break away, enter blood or lymph vessels, travel and start new tumours (secondary tumours) in organs such as the lungs, liver, bones or brain. This is what makes cancer most dangerous.
Cancers are named by where they start: carcinoma (skin and linings), sarcoma (bone, muscle), leukaemia (blood-forming cells), lymphoma (lymph system).
Risk factors: genetic and environmental
Anything that causes cancer is a carcinogen. A risk factor makes cancer more likely; it does not make it certain.
- Tobacco smoke (and chewing tobacco): over 60 carcinogens; linked to lung, mouth, throat, bladder and many more cancers. The biggest preventable cause worldwide.
- UV radiation from the Sun and tanning beds: damages skin-cell DNA; causes skin cancers including melanoma.
- X-rays, gamma rays and radon gas (ionising radiation): break DNA. Medical X-rays use tiny, controlled doses.
- Viruses: HPV (cervical, throat), hepatitis B and C (liver). Bacteria: H. pylori (stomach).
- Chemicals and pollution: asbestos, benzene, polluted air (fine particles), arsenic in water.
- Diet and lifestyle: alcohol, obesity, lots of processed/red meat, low fibre, little exercise.
- Genetic factors: some people inherit one faulty copy of a gene (for example BRCA1/BRCA2 for breast and ovarian cancer), so fewer extra mutations are needed. Age also matters: copying mistakes add up over time.
Cancer is not contagious. You cannot catch it from a person (only some cancer-causing viruses can pass between people).
Prevention, detection and treatment
Doctors estimate that 30–50% of cancers could be prevented:
- no tobacco in any form, little or no alcohol;
- sun protection: shade, clothing, sunscreen; no tanning beds;
- vaccines: HPV and hepatitis B;
- healthy weight, fruits, vegetables and whole grains, daily exercise;
- safety at work (masks, protective gear), clean air.
Early warning signs: a lump, a sore that does not heal, a mole that changes, unusual bleeding, long-lasting cough or weight loss without reason. Then see a doctor.
Screening finds cancer before symptoms: Pap/HPV test, mammogram, colonoscopy, skin checks. A biopsy (a tiny tissue sample under a microscope) confirms it.
Treatment: surgery (remove the tumour), radiotherapy (radiation aimed at the tumour), chemotherapy (drugs that kill fast-dividing cells, so hair and gut cells are hit too, causing side effects), targeted therapy (drugs that block a cancer's specific mutation) and immunotherapy (helping the immune system attack cancer cells).
Try it: the doubling game
Take a sheet of paper. Fold it in half: 2 layers. Again: 4. Keep going and count. After 7 folds (128 layers) you cannot fold any more. That is what doubling does: it starts slowly and then explodes. A tumour that doubles every 2 months goes from 1 cell to about 1 billion cells (30 doublings) in 5 years, which is why early detection matters. Try the divisions slider in the 3D.
Key formulas and definitions
- Number of cells after n divisions = 2ⁿ
- Mutation in control genes → uncontrolled mitosis → tumour
- Oncogene = accelerator stuck ON; tumour-suppressor gene = broken brake
- Benign = stays in capsule; malignant = invades + metastasis
- Carcinogen = anything that causes cancer (smoke, UV, X-rays, some chemicals and viruses)
Worked examples
1. One faulty cell divides every day. How many cancer cells after 10 days?
Cells = 2ⁿ = 2¹⁰ = 1024 cells.
2. A tumour cell doubles every 3 months. About how long to reach 1 billion cells (≈ 2³⁰)?
It needs 30 doublings. Time = 30 × 3 months = 90 months = 7.5 years. Cancers can grow silently for years, so screening helps.
3. Why is a mutation in a tumour-suppressor gene like p53 dangerous?
p53 is a brake: it stops the cycle when DNA is damaged and can trigger apoptosis. If p53 is broken, damaged cells keep dividing and more mutations pile up. Faulty p53 is found in about half of all cancers.
4. A doctor finds a slow-growing lump with a clear edge inside a capsule, with no spread. What type is it?
Benign: slow, encapsulated, no invasion or metastasis. It is usually removed by surgery and does not come back elsewhere.
5. Chemotherapy drugs often cause hair loss. Use cell division to explain why.
Many chemo drugs attack cells that divide fast. Cancer cells divide fast, but so do hair-root cells, gut lining and bone marrow. These normal fast cells are also damaged, causing hair loss, nausea and low blood counts.
Common mistakes
- Thinking cancer is caused by germs that spread from person to person. Cancer is not contagious; it comes from mutations in a person's own cells.
- Thinking every tumour is cancer. Benign tumours do not invade or spread; only malignant tumours are cancer.
- Thinking one mutation is enough. Usually several mutations in control genes must build up in the same cell.
- Thinking all cancer is inherited. Only about 5–10% are strongly linked to inherited genes; most come from mutations gained during life.