Understanding cancer: how it develops and spreads

Cancer starts in cells

The body is made of trillions of cells that normally grow, divide and die in a carefully controlled way. Instructions for this are held in each cell's DNA — its genetic code. Cancer begins when changes, called mutations, build up in the genes that control how a cell grows and when it should stop or die. Instead of behaving normally, the cell ignores the usual signals, keeps dividing, and refuses to die when it should. These faulty cells pass their broken instructions on to their offspring. It usually takes several such changes accumulating over time, which is one reason many cancers become more common with age, as damage adds up across the years.

Why gene changes happen

Most mutations are not inherited; they build up during life. Some occur simply as random errors when cells copy their DNA to divide — bad luck that increases with the sheer number of divisions over a lifetime. Others are driven by things that damage DNA: tobacco smoke, ultraviolet light from the sun and sunbeds, certain infections, some chemicals, obesity and alcohol. A minority of cancers stem from a faulty gene inherited from a parent, which raises risk but does not guarantee cancer. This is why prevention focuses on reducing avoidable damage — not smoking, sun protection, a healthy weight, limiting alcohol and vaccination against cancer-linked infections — while accepting that some cancers arise despite everything.

How a tumour forms and grows

When a cell starts dividing uncontrollably, it can form a lump called a tumour. Not all tumours are cancer: benign tumours grow in one place and do not invade or spread, whereas malignant (cancerous) tumours can invade nearby tissues and spread further afield. As a cancer grows, it needs a blood supply, so it can trick the body into building new blood vessels to feed it — a process called angiogenesis. Cancers also develop ways to hide from the immune system, which would otherwise destroy abnormal cells. These abilities — invading, recruiting a blood supply and evading defences — are hallmarks that separate cancer from ordinary overgrowth and explain why it can be so persistent.

How cancer spreads

The feature that makes cancer dangerous is its ability to spread, known as metastasis. Cancer can spread in three main ways: directly invading neighbouring tissues, travelling through the lymphatic system to nearby lymph nodes, or entering the bloodstream and lodging in distant organs such as the liver, lungs, bones or brain. When cancer spreads, the new deposits are still made of the original cancer's cells — so breast cancer that spreads to the bone is still breast cancer, not bone cancer, and is treated as such. Whether and how far a cancer has spread — its "stage" — is one of the most important things doctors work out, because it strongly shapes treatment and outlook.

Why this shapes prevention and treatment

Understanding the biology explains everything that follows. Because cancer builds up over years, screening programmes — for bowel, breast and cervical cancer in the UK — aim to catch it early or even before it starts, when it is far more curable. Because early cancer is more treatable than spread cancer, noticing warning symptoms and getting checked promptly matters enormously. Treatments target different weaknesses: surgery removes localised tumours, radiotherapy damages cancer cells' DNA, chemotherapy attacks rapidly dividing cells, and newer targeted and immunotherapy treatments exploit specific faults or unmask the cancer to the immune system. Knowing how cancer works turns a frightening mystery into a set of understandable problems that modern medicine increasingly knows how to tackle.