How Cancer Starts

Cancer is mostly a disease of older age. Yet in October 2026, the World Cancer Research Fund reported that several cancers are rising among people under fifty in England, the United States and the Netherlands.

Early-onset cancer is still uncommon, and the researchers say its causes are not fully understood. But it raises a question: why does age matter so much in the first place?

To answer that, we have to go inside the body, to a single cell that stops taking orders.

Your body holds about thirty trillion human cells. Many of them wear out, and every day around fifty to seventy billion are retired on purpose, in a tidy process called apoptosis.

Neighbours divide to fill the gaps. When a wound has healed, they slow down again. Each cell divides only when the body asks, and stops when it is told.

That is the bargain that keeps a body in shape. Cancer begins when one cell breaks it.

The rules are written in DNA, and every time a cell divides it must copy all of it. Cells check and repair their copies, but now and then a mistake slips through. That lasting change is a mutation.

According to the US National Cancer Institute, most cancers come from changes like these that pile up by chance over many years. Some are speeded up by carcinogens: tobacco smoke, ultraviolet light, certain viruses.

Only up to one in ten cancers is linked to a change inherited from a parent.

Which mistakes matter? Think of a cell as a car. Some genes are the accelerator: they push the cell to divide when growth is needed.

In 1976, Harold Varmus, J. Michael Bishop and Dominique Stehelin showed that a cancer-causing gene carried by a virus that gives chickens tumours was nearly identical to a gene in the normal cells of healthy birds. The virus had picked it up from its host. Cancer genes are faulty versions of our own.

A mutation can jam that accelerator down. Watch one cell keep dividing after its neighbours have stopped.

Other genes are the brakes, called tumour suppressors. We carry two copies of each, one from each parent, and one working copy is usually enough to stop the car. A “hit” here means a mutation that breaks one copy.

In 1971, Alfred Knudson studied a rare eye cancer in children. Inherited cases came younger, often in both eyes. His explanation: it takes two hits, one to each copy, and some children are born with the first hit already.

Watch twenty lives unfold. Those born with one broken copy reach their second hit much sooner.

One brake matters more than most. A protein called p53, identified in 1979, watches for damaged DNA.

When it finds damage, it halts the cell until the damage is repaired, or, if the damage is too great, it tells the cell to destroy itself. The yellow cells here are damaged; watch them vanish or recover.

Now break p53. Damaged cells survive and divide, passing their mistakes on. It is no surprise that p53 is mutated in roughly half of all tumours.

One stuck accelerator or one broken brake is rarely enough. A cell usually needs several hits in the right genes.

Bowel cancer shows the path most clearly. In a model proposed in 1990, a brake gene called APC fails first and a small growth called a polyp appears. Later, an accelerator gene, KRAS, and then p53 are hit.

Each step takes time. Studies estimate that going from a polyp to cancer typically takes more than a decade.

Even a rogue cell faces another limit. In 1961, Leonard Hayflick found that normal human cells in a dish divide roughly forty to sixty times, then stop.

The clock is at the ends of each chromosome. Caps called telomeres lose a little length with every copy, and when they get too short, the cell retires.

Most cancer cells cheat by switching on an enzyme, telomerase, that rebuilds the caps. Switch it on, and the counter never runs out.

A growing clump of cells soon runs short of food and oxygen. Without a blood supply it stays a tiny, pinhead-sized sphere.

In 1971, the surgeon Judah Folkman proposed that tumours send out signals that make new blood vessels grow toward them. Watch the vessels arrive, and the tumour start to swell.

He also suggested that blocking those signals could keep tumours small, an idea that later led to new medicines.

Not every tumour is cancer. A benign growth stays where it started. It can grow large and press on its neighbours, but it does not spread.

A malignant tumour invades the tissue around it. Its cells can slip into the bloodstream or the lymphatic system and settle in distant organs. This is metastasis.

Even far from home, the cells keep their origin. Breast cancer that has spread to the lungs still looks and behaves like breast cancer.

In 2000, Douglas Hanahan and Robert Weinberg gathered these tricks into a list they called the hallmarks of cancer: abilities that almost every cancer must acquire, whatever the organ.

Making its own go signals. Ignoring stop signals. Escaping self-destruction. Dividing without limit. Building blood vessels. Invading and spreading.

Later updates added rewiring the cell's energy use and hiding from the immune system.

Now we can answer the opening question. If a cell needs several rare hits, and hits arrive at a steady rate, then the chance that some cell has collected them all rises steeply with age.

Each dot is a family of cells descended from one ancestor. Move through the ages and watch the red dots, families with four hits, our stand-in for enough, stay rare for decades and then multiply.

That is what the statistics show. In the UK, more than half of new cancers are diagnosed in people aged seventy and over.

Worldwide, about twenty million people were diagnosed with cancer in 2022, and about nine point seven million died of it.

Many hits are bad luck. But in February 2026, the World Health Organization's cancer agency estimated that thirty-seven per cent of new cases were linked to preventable causes.

Tobacco led, linked to about fifteen per cent of all cases, then infections such as HPV and hepatitis at ten, and alcohol at three. Those are carcinogens raising the rate of hits.

So what about younger adults? If more people are collecting hits earlier, cancers that usually wait until old age would start to appear sooner.

The analysis points to obesity, diet, inactivity, alcohol and smoking, and possibly the environment, while lung cancer in the young is falling as smoking declines. Some of the rise is better detection.

No one yet knows the full answer. A new British trial of a quarter of a million people aims to separate the causes.

Cancer is not an invader. It is one of our own cells that, hit by hit, has jammed its accelerator and lost its brakes, its guardian and its countdown, then learned to feed itself and travel.

That takes many rare accidents, which is why it usually takes decades, and why the body stops almost every faulty cell long before.

Why some younger adults now seem to collect their hits sooner is still an open question. Each step in this film is a place where researchers are looking for the answer.