In 1971 Richard Nixon announced a "war on cancer", hoping that the same combination of big science and big government that had put astronauts on the Moon could defeat the disease within a few years. Cancer kills roughly 10m people a year worldwide—about one in six of all deaths. In America it is the second-most-common cause of death, behind heart disease, killing around 600,000 people a year. In rich countries half of men and one in three women develop it at some point. In countries including Australia, Britain, Canada and Japan it is the leading cause of death. Yet, adjusted for population growth and ageing, the early 1990s proved an inflection point: since then the age-adjusted death rate has been falling steadily, year after year. In America the rate is now about a third lower than in the 1990s. The trend is similar across the developed world.
Some victories have been spectacular. Childhood leukaemia, once virtually a death sentence, now has a five-year survival rate above 90%. Yet because cancer is not one illness but a whole category, much of the progress has come not from big breakthroughs but from thousands of smaller advances in screening, surgery and drugs.
The biggest advances have come from reductions in smoking, which causes around 85% of lung cancers and 20% of all cancer deaths globally. Screening programmes—mammograms, colonoscopies and cervical smears—have helped detect pre-cancerous tissue early enough to remove it. Better surgery and medicines have improved survival rates, and immunotherapy has made big strides in recent years.
By one estimate, nearly 6m deaths were averted in America between 1975 and 2020 from lung, breast, bowel, prostate and cervical cancer (which together accounted for about 70% of cancer deaths in the late 1970s). Just over half of the averted deaths were the result of reduced smoking, 23% stemmed from better screening and 20% from improved treatment.
Stomach cancer has also declined sharply in rich countries. In the 1990s researchers established that it was often caused by Helicobacter pylori, a bacterium whose prevalence was already falling thanks to improved hygiene and greater antibiotic use since the 1950s. The discovery spurred direct testing and treatment.
Cervical cancer once killed more women in America than any other form of the disease. The first gains came from screening programmes that detected and removed suspect tissue. Studying the many samples collected in this way led to the discovery that almost all cervical cancers were caused by the human papillomavirus (HPV). HPV vaccines now hold out the prospect of near-eradication. In 2008 Britain began offering the vaccine to teenage girls; a decade and a half later, rates of cervical cancer among women in their 20s are down by 90%, and British health officials talk of virtually eradicating cervical cancer by 2040. A cheaper version of the vaccine, developed in India, now underpins a mass-vaccination campaign there.
Cancer typically develops slowly: genetic mutations cause abnormal cells to reproduce, eventually forming lesions, polyps or tumours that can take 5–15 years to grow. Yet only about 25% of the most common breast-tissue lesions turn cancerous, and only 5–10% of bowel polyps develop into cancer. Scientists at University College London have found that 30% of a particular lung-lesion type regress if left alone. Because there is no reliable way to predict which lesions will turn malignant, many patients undergo unnecessary surgery, radiation or chemotherapy.
Some 5–10% of cancer cases have genetic origins. About one in 200 people carries faults in BRCA-1 and -2 genes, conferring a 60–80% risk of breast or ovarian cancer. One in 300 has Lynch syndrome—mutations in DNA-repair genes—carrying a 40–80% chance of colorectal, endometrial and other cancers.
Biobanks from large studies such as the EPIC project, which has tracked 500,000 Europeans for nearly 30 years, have enabled researchers to examine blood from participants who later developed cancer against samples from those who stayed healthy. Such work has found that high levels of insulin-like growth factor raise the risk of breast and bowel cancer, and a team led by Marc Gunter at Imperial College London has identified new protein biomarkers for breast cancer.
Genetic screening, blood tests and lifestyle data are now being fed into "multimodal" cancer-risk calculators that have entered clinical practice in the past five years.
Several groups in America and Europe are testing preventive vaccines for breast, bowel and other cancers in high-risk patients (those with BRCA faults, Lynch syndrome or pre-cancerous lesions). First results, showing whether they reduce the recurrence of polyps or other lesions, are expected in three to five years.
Oxford University researchers have developed a vaccine targeting specific changes in the lung cells of smokers that are linked to cancer, due to begin clinical trials in 2026. Nouscom, a Swiss biotech company, has developed a vaccine targeting 209 different molecular fragments found in pre-cancerous and cancerous tissue; a first round of clinical trials reported in April 2025 showed it successfully induces an immune response against cancer cells. A vaccine targeting the protein MUC1, found in 80% of all cancer types, showed a 38% reduction in polyp recurrence within a year in a sub-group of people with colon polyps, according to preliminary results published in 2023.
Researchers have noticed that people who take aspirin for heart-attack prevention or metformin for diabetes have reduced cancer rates. In 2023 Britain's drug regulator approved anastrozole, a breast-cancer treatment drug, for prophylactic use after clinical trials showed it halves the risk of breast cancer in some post-menopausal women. There is hope that GLP-1 receptor agonists such as Ozempic might also help prevent certain cancers.
In 2023 researchers found that metformin can reduce cancer recurrence for women treated for one particular form of breast cancer (about 20% of cases), but not for other types—illustrating a broader trend toward sub-group-specific preventive therapies rather than one-size-fits-all solutions.
Scientists have found that so-called cancer-driver mutations are surprisingly common in healthy tissue. Such mutations appear in around a quarter of healthy skin cells. By middle age more than half the surface of the oesophagus and nearly 10% of the lining of the stomach is covered by cells with cancer-driver mutations. These populations have also been confirmed in the colon, lungs and ovaries.
Why these primed cells do not grow into tumours appears to come down to cellular competition. As cells divide on the outermost layers of organs, those best adapted to their environments push out the rest, which are shed from the tissue. Cells possessing specific beneficial mutations have been shown in mice to displace neighbours carrying cancer-driver mutations, as well as tiny tumours with fewer than 100 cells. Blood samples taken from people as they age show that the number of cells with cancer-driver mutations waxes and wanes over time, suggesting the competition plays out over years.
Phil Jones, a researcher at the Wellcome Sanger Institute in Britain, found that cells with cancer-driving mutations in PIK3CA, a gene that regulates cell growth and survival, undergo metabolic changes that help them outcompete non-mutated cells. In trials involving mice, published in August 2024 in Nature Genetics, his team found that metformin introduced the same metabolic change in non-mutated cells within the oesophagus, halting the growth of PIK3CA-mutated cells. Conversely, when mice were fed a high-fat diet, troublesome cells thrived; they were also more numerous in people with obesity, suggesting interventions targeting the condition could prevent oesophageal cancer.
Identifying beneficial mutations is complicated by the fact that the human body possesses thousands of different cell types with different molecular machinery. A mutation found to reduce the risk of cancer in the oesophagus, for example, has been shown in other studies to have no such effect on the skin. Techniques are improving: using CRISPR, Dr Jones says his team can now test 15,000 genes in three months, compared with the years previously needed to breed mice with artificially modified DNA.
A study published in 2020 by Allan Balmain of the University of California in San Francisco found that only three of 20 chemicals known or suspected to be human carcinogens actually induced mutations in mice; most appeared instead to promote tumour growth in other ways. This suggests that 80-90% of carcinogens to which people are exposed may not induce mutations at all.
These non-mutagenic carcinogens instead seem to exploit the body's immune system. Frequent exposure can lead to chronic inflammation, which encourages cancer-driver cells to develop into full-blown tumours. Inflammation dispatches immune cells to the site of an injury, removing irritants and triggering tissue growth. But when deployed against persistent irritants—such as air-pollution particles in the lungs—inflammation can itself damage tissue and lead to tumour formation. In this sense, tumours have been likened to wounds that never heal.
A study published in Nature in 2023 by a group led by Charles Swanton of the Francis Crick Institute in London found strong evidence that urban air pollution causes lung cancers in non-smokers. In mice, air pollution led to inflammation in the lungs, which caused surrounding cells with a mutation characteristic of such cancers to grow and form tumours. The researchers estimated that living for as little as three years in a place with heavy air pollution may be enough to tip such cells into a tumour-growing phase. The researchers identified an immune-system protein called interleukin-1ß as the enabler of the inflammation that stoked tumour development; in mice, drugs that blocked interleukin-1ß suppressed tumour formation when the animals were exposed to air pollution. Chronic inflammation has also been shown to boost the spread of cells with harmful mutations in response to acid reflux, ultraviolet solar radiation and persistent gut infection with certain bacteria.
These discoveries are forcing clinicians to rethink cancer prevention. Increasingly researchers think the best way to stop cancers might be to target the immune system rather than cancerous mutations themselves—developing drugs that help the body limit the harm done by its own inflammatory responses. Such drugs could be game-changing for people with a high risk of developing cancer, including those with faulty BRCA genes, former smokers, cancer survivors and those with pre-cancerous tissues such as colon polyps or not-yet-malignant lesions.
A report published in Nature Medicine on February 3rd 2026, led by researchers at the International Agency for Research on Cancer at the World Health Organisation, provided the most comprehensive figures to date on preventable cancers. The study covered 30 risk factors—including habits such as smoking and alcohol consumption, as well as environmental factors such as air pollution and infections—and found that of the nearly 20m new cancers thought to have occurred worldwide in 2022, 38% were due to preventable factors. The authors estimate the real figure may be somewhat higher, as the study excluded various suspected carcinogens such as certain food preservatives.
Two risk factors stand out virtually everywhere: tobacco smoking and infections. Smoking is the leading cause of cancers in men in almost all countries outside sub-Saharan Africa, as well as for women in America, Europe and Oceania. Infections are the leading cause for women elsewhere. All told, one in six cancers worldwide are caused by smoking and one in ten by an infection. Alcohol, third in the overall ranking, causes 4.6% of all cancers in men and 1.6% of those in women. Smoking has been linked to at least 15 types of cancer, and even those who quit can have a heightened risk of developing cancer for decades afterwards. Many countries are therefore trying to catch lung cancer earlier by introducing routine CT scans for both current and former smokers.
Nearly all cervical cancers are caused by chronic infection with the human papillomavirus (HPV). Liver cancers arise predominantly from the Hepatitis B and C viruses. Stomach cancers are mostly caused by infection with Helicobacter pylori. Vaccines against HPV and Hepatitis B, now part of many countries' routine jabs for children, are forecast to prevent millions of cancers in the coming years. Although there is no vaccine for Hepatitis C, highly effective antiviral treatments have become available in the past ten years. Early-life infection with H. pylori remains widespread in poorer countries, where stomach cancer is much more common.
In 2025 China overtook America as the main source of cancer research.
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