Cancer is a group of diseases in which cells divide uncontrollably, producing masses of abnormal tissue called tumours. At the molecular level, cancer always begins with damage to the genes that regulate cell division — genes that normally act as the brakes and accelerators of the cell cycle. Understanding this mechanism is central to GCSE biology.
What is the cell cycle and how is it normally controlled?
Body cells normally divide by mitosis to produce two genetically identical daughter cells for growth and repair. The process is tightly regulated by a network of proteins encoded by specific genes:
- Proto-oncogenes — promote cell division (the accelerators). When mutated into oncogenes, they send constant "divide now" signals.
- Tumour suppressor genes — slow or stop cell division (the brakes). When inactivated by mutation, the brakes fail.
Cancer typically requires multiple mutations — in oncogenes, tumour suppressor genes, and genes controlling DNA repair — to develop. This is why cancer risk increases with age (time for mutations to accumulate) and with exposure to mutagens.
What is the difference between a benign and a malignant tumour?
Not every tumour is cancer.
| Feature | Benign tumour | Malignant tumour (cancer) |
|---|---|---|
| Growth rate | Usually slow | Usually faster |
| Boundary | Distinct; often has a capsule | Irregular; invades surrounding tissue |
| Spread | Does not spread to other sites | Can metastasise (spread via blood/lymph) |
| Danger | Usually not life-threatening (may press on structures) | Potentially life-threatening |
| Example | Lipoma (fatty lump), most moles | Carcinoma, sarcoma, leukaemia |
Benign tumours are removed if they cause problems but are not classified as cancer. Malignant tumours can invade surrounding healthy tissue and shed cells that travel to distant organs to form secondary tumours — this process is called metastasis and greatly complicates treatment.
What are the risk factors for cancer?
A risk factor increases the probability of developing cancer but does not guarantee it. Risk factors either increase the chance of mutations or impair the body's ability to detect and destroy abnormal cells.
| Risk factor | Type of cancer(s) most associated |
|---|---|
| Smoking | Lung, throat, bladder, kidney cancers |
| UV radiation (sunlight / sunbeds) | Skin cancer (melanoma) |
| Ionising radiation (X-rays, gamma rays, radon gas) | Leukaemia, thyroid cancer |
| Carcinogens (chemicals in tobacco, certain dyes) | Various |
| Certain viruses — HPV (human papillomavirus) | Cervical cancer |
| Alcohol | Liver, breast, bowel cancers |
| Inherited genetic mutations (e.g. BRCA1/2) | Breast, ovarian cancers |
Having a risk factor raises statistical probability — it does not mean a person will definitely develop cancer, and people without any known risk factors still develop cancer due to random mutations.
How is cancer treated?
Several treatment approaches exist, often used in combination:
- Surgery — removes the tumour. Effective when the cancer is localised and has not spread. Surgeons aim to remove the tumour plus a margin of healthy tissue.
- Radiotherapy — high-energy radiation (gamma rays or X-rays) is aimed at the tumour to damage the DNA of cancer cells, preventing further division. Surrounding healthy tissue is partially shielded or the radiation beam is rotated to concentrate the dose on the tumour.
- Chemotherapy — drugs that interfere with cell division (e.g. by blocking DNA replication) are administered. Because chemotherapy targets rapidly dividing cells, it also affects normal fast-dividing cells such as hair follicles and gut lining, causing side effects including hair loss and nausea.
- Immunotherapy — harnesses the immune system to recognise and destroy cancer cells. For example, checkpoint inhibitors block proteins that cancer cells use to "hide" from immune cells.
- Targeted therapy — drugs designed to block specific molecular signals that drive growth of a particular cancer (e.g. Herceptin targets HER2-positive breast cancer cells).
How does cancer spread through the body?
Metastasis occurs when malignant cells break away from the primary tumour and travel via the bloodstream or lymphatic system to other organs, where they establish secondary tumours. Common sites for metastasis include the liver, lungs, bone, and brain. Secondary tumours retain characteristics of the original cancer (e.g. cells from a primary lung cancer that spread to the liver still behave like lung cancer cells), which helps doctors choose appropriate treatment.
Why is early detection important?
The smaller a tumour when detected, the less likely it is to have metastasised and the more treatment options are available. This underpins national screening programmes: cervical smear tests detect pre-cancerous cell changes caused by HPV; mammography detects breast tumours; bowel cancer screening detects blood in stool or polyps before they become cancerous.
Frequently asked questions
Is cancer inherited?
Most cancers are not directly inherited — they arise from random mutations in body cells during a person's lifetime (somatic mutations), influenced by environmental risk factors. However, some inherited gene variants substantially raise the risk: mutations in the BRCA1 or BRCA2 tumour suppressor genes increase lifetime risk of breast and ovarian cancer significantly. These inherited variants account for roughly 5–10 % of breast cancers. Having an inherited predisposition does not guarantee cancer will develop, but screening and preventive measures become especially important.
Why does chemotherapy cause hair loss?
Chemotherapy drugs target rapidly dividing cells. Cancer cells divide rapidly, but so do the cells of hair follicles, the gut lining, and bone marrow. When chemotherapy drugs damage these normal rapidly dividing cells, hair falls out, the gut becomes inflamed (nausea, mouth ulcers), and blood cell production drops (increasing infection risk). Hair loss from chemotherapy is almost always temporary — follicle cells recover once treatment ends.
What is the difference between a mutation and cancer?
A mutation is any change in the base sequence of DNA. Most mutations are harmless (in non-coding regions), are corrected by DNA repair enzymes, or cause the affected cell to undergo programmed cell death (apoptosis). Cancer only results when mutations accumulate in the specific genes that control cell division — proto-oncogenes and tumour suppressor genes — and when the cell evades all the normal checkpoints that would otherwise eliminate it. A single mutation almost never causes cancer.
How does UV radiation cause skin cancer?
Ultraviolet radiation from the sun or sunbeds carries enough energy to directly damage DNA in skin cells — specifically causing adjacent thymine bases to bond together, forming thymine dimers that distort the DNA strand. If DNA repair mechanisms fail to correct these dimers before the cell divides, the mutation is copied into daughter cells. Repeated UV exposure leads to accumulated mutations in skin cells; if these mutations affect oncogenes or tumour suppressor genes, the result can be melanoma or other skin cancers.
For Socratic GCSE biology with Professor Darwin — connecting cell, tissue, and organism-level explanations of cancer — visit aitutors.me.