# How Cancer Starts > A new analysis reports several cancers rising among people under fifty, even though most cancers still strike older people. To see why age matters so much, this film follows one cell: how the body balances division and death, how DNA copying errors and carcinogens create mutations, why cancer needs both a stuck accelerator and broken brakes, what the guardian protein p53 does, why hits pile up with age, and the tricks a tumour needs to become dangerous: immortality, its own blood supply and the ability to spread. Seed a rogue cell, break p53, run Knudson’s two-hit lives and switch on telomerase yourself. Education, not medical advice. Interactive film: https://www.planetpast.com/stories/how-cancer-starts/ Publisher: PlanetPast (https://www.planetpast.com/) · d => T('readPublished', l, { d: dateIn(d, l) }) 2026-10-16 · Biology, Chemistry ## Prologue ### The cell that won’t stop *Mistakes, years and one rogue cell* More than a hundred diseases, one way to begin. 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. - **3.9 → 8.4**: bowel cancer per 100,000 under-50s, 2001 → 2023 - **7**: cancer types with significant rises - obesity, diet, inactivity, alcohol, smoking - possibly environmental exposures - partly better awareness and earlier diagnosis - lung cancer in under-50s is falling ![The median age at diagnosis is above 60. AI-generated still.](https://assets.planetpast.com/a/93/931c95ab5a93ac4e.jpg) Prologue · The news #### Cancer in younger adults A World Cancer Research Fund analysis published in October 2026 found significant rises in early-onset cancer (diagnosed under 50) for seven cancer types in England, five in the US and four in the Netherlands. In England, bowel cancer in under-50s rose from 3.9 to 8.4 per 100,000 between 2001 and 2023. The researchers say causes are not fully understood; better detection may explain part of the rise but, they say, not all of it. This film explains how cancer starts. It is education, not medical advice: questions about your own health belong with a doctor. How to use: pick a chapter or press ← →; drag to rotate. Ten steps have buttons you can press. Sources: [Irish Examiner / The Guardian: cancer rates rising more quickly among younger people, WCRF analysis (6 Oct 2026)](https://www.irishexaminer.com/world/arid-41920237.html); [Tasnim News: cancer rates rising faster among younger people, international study finds (6 Oct 2026)](https://www.tasnimnews.ir/en/news/2026/10/06/3716317/cancer-rates-rising-faster-among-younger-people-international-study-finds/amp) ## Chapter I · The bargain ### Divide only when asked *Chapter I · The bargain* A body is a society of cells that follow the rules. 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. - **~30 trillion**: human cells (Sender, Fuchs & Milo, 2016) - **50–70 billion**: cells lost to apoptosis per day ![Linings like the gut are rebuilt continually: new cells form below as old ones are shed. AI-generated illustration.](https://assets.planetpast.com/a/83/833a6102557e2c66.jpg) - divide only on a signal - stop when crowded - self-destruct if badly damaged - stay in your own tissue Chapter I · The bargain #### Cell turnover A 2016 study by Sender, Fuchs and Milo estimated about 30 trillion human cells in a body. The average adult loses roughly 50 to 70 billion cells a day to apoptosis, a regulated form of cell death. Normal cells divide to replace worn-out or injured cells and return to their usual rate once a wound heals. The 3D models are schematic and use illustrative numbers. Sources: [Medical News Today: how many cells are in the human body? (Sender, Fuchs & Milo, 2016)](https://www.medicalnewstoday.com/articles/318342); [Wikipedia: Apoptosis](https://en.wikipedia.org/wiki/Apoptosis); [NCI SEER Training: what is cancer?](https://training.seer.cancer.gov/disease/cancer/) ### A typo in the instructions *Chapter I · The bargain* Mutations are mostly accidents. 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. - random copying mistakes - damage from carcinogens - inherited from a parent (rarer) ![UV light can kink a DNA strand; if it is copied before it is repaired, the error becomes permanent. AI-generated illustration.](https://assets.planetpast.com/a/62/62d368d3414be5cf.jpg) - **up to 10%**: of cancers may be caused by inherited genetic changes (NCI) Chapter I · The bargain #### Cancer is a genetic disease The National Cancer Institute calls cancer a genetic disease: it is caused by changes to genes that control how cells grow and multiply. These arise from random mistakes during cell division, from carcinogens such as tobacco smoke, UV rays and HPV, or are inherited. “The vast majority of cancers occur by chance”; up to 10% may be caused by inherited changes. The 3D models are schematic and use illustrative numbers. Sources: [National Cancer Institute: the genetics of cancer](https://www.cancer.gov/about-cancer/causes-prevention/genetics) ## Chapter II · Accelerator and brakes ### The accelerator *Chapter II · Accelerator and brakes* Cancer genes were our own genes all along. 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. ![Rous sarcoma virus carries the SRC gene; the same gene turned up in fish and mammals, including humans. AI-generated illustration.](https://assets.planetpast.com/a/be/be31a09b86e3aadc.jpg) - **SRC**: the first oncogene found; its normal version is called a proto-oncogene - normal: growth on demand - mutated: growth signal stuck “on” - the virus copied it from a host cell Chapter II · Accelerator and brakes #### Oncogenes In 1976 Varmus, Bishop and Stehelin reported in Nature that SRC, the oncogene of Rous sarcoma virus, “was nearly identical to a sequence in the normal cellular DNA” of several bird species: the virus had picked up a host gene. Bishop and Varmus shared the 1989 Nobel Prize “for their discovery of the cellular origin of retroviral oncogenes”. The accelerator-and-brakes picture is a teaching analogy. The 3D models are schematic and use illustrative numbers. Sources: [US National Library of Medicine: retroviruses and the genetic origins of cancer, 1970–1993](https://mhm.nlm.nih.gov/spotlight/mv/feature/oncogenes); [Nobel Prize in Physiology or Medicine 1989](https://www.nobelprize.org/prizes/medicine/1989/summary/) ### The brakes *Chapter II · Accelerator and brakes* Why some families get cancer younger. 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. - the cell’s brakes - two copies, one from each parent - both must fail before control is lost - inherited: first hit present from birth; younger, often both eyes - sporadic: both hits acquired during life; later onset - later: the gene was identified as RB1 $$P_{\text{one hit already}} \approx p$$ $$P_{\text{none yet}} \approx p^{2}$$ - $p$: small chance that a given copy is hit Chapter II · Accelerator and brakes #### Knudson’s two-hit hypothesis Alfred G. Knudson proposed in 1971, from a statistical study of retinoblastoma, that two hits to DNA are needed. In inherited cases one hit is present from birth, so only one more is needed; sporadic cases need two acquired hits, which explains their later onset. The gene was later identified as RB1. In the grid, the hit rate is invented for illustration; real retinoblastoma is rare. Sources: [Wikipedia: Two-hit hypothesis](https://en.wikipedia.org/wiki/Two-hit_hypothesis) ### The guardian *Chapter II · Accelerator and brakes* One protein decides: repair or self-destruct. 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. - senses DNA damage - pauses the cell cycle for repair - triggers apoptosis if repair fails - **1979**: first identified - **~½**: of tumours carry p53 mutations Chapter II · Accelerator and brakes #### p53, guardian of the genome p53 is a protein of 53 kilodaltons first identified in 1979. Mutations in p53 appear in roughly half of all tumours, and it is now known as the “guardian of the genome”. The repair-or-remove choice in the model is simplified; real cells use many signals. The 3D models are schematic and use illustrative numbers. Sources: [HHMI BioInteractive: the p53 gene and cancer](https://media.hhmi.org/biointeractive/click/p53/01.html); [MedlinePlus Genetics: TP53 gene](https://medlineplus.gov/genetics/gene/tp53) ## Chapter III · Hit after hit ### One step at a time *Chapter III · Hit after hit* A single mutation is almost never enough. 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. - step 1: APC brake lost: a small polyp forms - step 2: KRAS accelerator jammed (in about 40% of tumours) - later: p53 lost (over 60% of cancers): cancer ![Many polyps never become cancer, and they can be found and removed early. AI-generated illustration.](https://assets.planetpast.com/a/6e/6e05d31aa7df07d3.jpg) - **~10–26 years**: range of estimated mean times Chapter III · Hit after hit #### A stepwise disease The Fearon–Vogelstein model (1990) holds that inactivation of the APC tumour suppressor occurs first in normal colonic tissue; activating KRAS mutations (found in about 40% of tumours) follow, and TP53 mutations (in over 60% of colorectal cancers) are late events. A review estimates a mean of 10.6 to 25.8 years from adenoma to cancer across all age groups. Not every bowel cancer follows this exact order; it is the classic model. Sources: [Review (PMC9924026): genetic progression of colorectal cancer](https://pmc.ncbi.nlm.nih.gov/articles/PMC9924026/) ## Chapter IV · The tumour’s tricks ### Cheating the countdown *Chapter IV · The tumour’s tricks* Normal cells can only divide so many times. 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. - **40–60**: divisions before normal human cells stop, in culture - repeated DNA at chromosome ends - a little is lost at every copy - too short → the cell becomes senescent ![With telomerase active, the caps stay long, one of the hallmarks called replicative immortality. AI-generated illustration.](https://assets.planetpast.com/a/07/0740df495dcb2677.jpg) Chapter IV · The tumour’s tricks #### Replicative immortality Leonard Hayflick advanced the concept in 1961: normal human fetal cell populations divide roughly 40 to 60 times in culture before senescence. The limit correlates with telomere length, which shrinks with each replication. Most cancer cells do not senesce because they express telomerase, which extends telomeres. The 3D models are schematic and use illustrative numbers. Sources: [Wikipedia: Hayflick limit](https://en.wikipedia.org/wiki/Hayflick_limit); [AACR: updated hallmarks of cancer (2022)](https://www.aacr.org/blog/2022/01/21/new-dimensions-in-cancer-biology-updated-hallmarks-of-cancer-published/) ### Its own blood supply *Chapter IV · The tumour’s tricks* Without vessels, a tumour stays tiny. 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. ![Folkman called the signal “tumour angiogenesis factor”. AI-generated illustration.](https://assets.planetpast.com/a/3b/3b038203e5c6dc20.jpg) - the growth of new blood vessels - normal in healing and growth - hijacked by tumours Chapter IV · The tumour’s tricks #### Angiogenesis In a 1971 paper in the New England Journal of Medicine, Judah Folkman proposed that tumours grow new blood vessels by releasing a signalling factor, and that blocking this process could keep tumours small. Without a blood supply, tumours stay as tiny, pinhead-size spheres. “New medicines” refers to anti-angiogenic drugs used for some cancers; this film does not discuss treatment choices. The 3D models are schematic and use illustrative numbers. Sources: [PBS NOVA: cancer warrior Judah Folkman](https://www.pbs.org/wgbh/nova/article/folkman-cancer) ### Crossing the wall *Chapter IV · The tumour’s tricks* What makes a tumour a cancer. 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. - stays in its original place - often enclosed in a capsule - may press on nearby structures ![To spread, a cell must leave the tumour, survive the journey and grow in a new tissue. AI-generated illustration.](https://assets.planetpast.com/a/a9/a990459d14331577.jpg) - **100+**: different diseases; each keeps the name of where it started, even after spreading Chapter IV · The tumour’s tricks #### Benign and malignant Benign growths stay in their original location; they may grow large and press on nearby structures but usually do not spread and are often enclosed in a capsule. Malignant tumours invade and destroy the tissue where they start, then spread and form new growths. Cancer keeps the characteristics of its organ of origin after it spreads. Cancer is more than 100 different diseases. The 3D models are schematic and use illustrative numbers. Sources: [NCI SEER Training: what is cancer?](https://training.seer.cancer.gov/disease/cancer/); [Cedars-Sinai: overview of cancer (spread through blood and lymph; naming by primary site)](https://www.cedars-sinai.org/health-topics/overview-of-cancer) ### The hallmarks *Chapter IV · The tumour’s tricks* One checklist for a hundred diseases. 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. - self-sufficient growth signals - insensitive to anti-growth signals - evading apoptosis · limitless division - sustained angiogenesis - tissue invasion and metastasis - 2011: energy metabolism, immune evasion as emerging hallmarks; inflammation as enabling - 2022: those two promoted to core hallmarks Chapter IV · The tumour’s tricks #### The hallmarks of cancer Hanahan and Weinberg’s original six hallmarks (2000): self-sufficiency in growth signals, insensitivity to growth-suppressive signals, evading programmed cell death, replicative immortality, sustained angiogenesis, and tissue invasion and metastasis. In 2011 they added reprogramming energy metabolism and evading immune destruction as emerging hallmarks, and tumour-promoting inflammation as an enabling characteristic; in 2022 the two emerging hallmarks became core hallmarks. Sources: [AACR: updated hallmarks of cancer (2022)](https://www.aacr.org/blog/2022/01/21/new-dimensions-in-cancer-biology-updated-hallmarks-of-cancer-published/) ## Chapter V · Who gets it ### Why age matters *Chapter V · Who gets it* Steady mistakes, steep risk. 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. $$P(\text{all } k \text{ hits by age } t) \;\propto\; t^{\,k}$$ - $k$: number of hits needed - $t$: age - **> ½**: of new cancers diagnosed at age 70+ - **85–89**: age group where incidence peaks Chapter V · Who gets it #### Age and cancer Cancer Research UK explains that DNA faults the body fails to repair accumulate over time, and each extra mutation makes a cell more likely to become cancerous. More than half of new UK cancer cases are diagnosed in people aged 70 and over, and incidence peaks at ages 85–89. It also notes that mutations alone do not explain everything: ageing brings other changes, such as more inflammation. The dot model and the t^k rule are rough illustrations. Sources: [Cancer Research UK: age, the forgotten cancer risk factor (2023)](https://news.cancerresearchuk.org/2023/05/29/age-the-forgotten-cancer-risk-factor/) ### Chance, and more than chance *Chapter V · Who gets it* Some hits we can avoid. 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. - **~20 million**: new cases - **~9.7 million**: deaths - all preventable causes: 37% - tobacco: 15% - infections: 10% - alcohol: 3% ![In men the WHO estimate rises to 45% of cases; in women it is 30%. AI-generated still.](https://assets.planetpast.com/a/84/84e9b412c896f4ed.jpg) Chapter V · Who gets it #### The global picture IARC’s GLOBOCAN estimates about 20 million new cancer cases and 9.7 million deaths in 2022. A WHO/IARC analysis released on 3 February 2026 linked 37% of new cases in 2022 (about 7.1 million) to 30 preventable causes, led by tobacco (15%), infections (10%) and alcohol (3%); 45% in men and 30% in women. These are population estimates, not personal risk figures. For personal advice, talk to a doctor. Sources: [UICC: GLOBOCAN 2022 global cancer data](https://www.uicc.org/news/globocan-2022-latest-global-cancer-data-shows-rising-incidence-and-stark-inequities); [WHO / IARC: four in ten cancer cases could be prevented globally (3 Feb 2026)](https://who.int/news/item/03-02-2026-four-in-ten-cancer-cases-could-be-prevented-globally) ### Back to the news *Chapter V · Who gets it* A real rise, a puzzle still open. 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. - kidney, 2000: 2.5 - kidney, 2023: 5.3 - obesity and diet - inactivity, alcohol, smoking - possibly environmental exposures - earlier detection (part of the rise) ![A King’s College London trial funded by Cancer Research UK will follow 250,000 people, focusing on bowel cancer. AI-generated still.](https://assets.planetpast.com/a/41/4103d01174752486.jpg) Chapter V · Who gets it #### Early-onset cancer In the US, early-onset kidney cancer rose from 2.5 to 5.3 per 100,000 between 2000 and 2023, and bowel, uterine and pancreatic cancers each rose by more than 50%. Lung cancer in under-50s fell in all three countries. The researchers list obesity, diet, inactivity, alcohol, smoking and possibly environmental exposures as likely contributors; the analysis does not establish causes. The first line of narration is a way of thinking about the trend, not a finding of the study. Sources: [Irish Examiner / The Guardian: cancer rates rising more quickly among younger people, WCRF analysis (6 Oct 2026)](https://www.irishexaminer.com/world/arid-41920237.html) ## Epilogue ### The cell that won’t stop *Epilogue* Many rare accidents, and an open question. 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. - jammed an accelerator (oncogene) - broken both copies of a brake - escaped p53 and self-destruction - rebuilt its telomeres - grown vessels, invaded, spread - 1961: Hayflick: normal cells divide 40–60 times - 1971: Knudson’s two hits; Folkman’s angiogenesis - 1976: SRC: cancer genes come from normal genes - 1979: p53 identified - 1990: stepwise model of bowel cancer - 2000: the hallmarks of cancer ![All stills and illustrations in this film are AI-generated.](https://assets.planetpast.com/a/6d/6d803a89272fee92.jpg) Epilogue · Sources #### How cancer starts Cancer arises when a cell accumulates changes in genes that control growth, division, repair and death, and then acquires the abilities summarised as the hallmarks of cancer. Age, chance, inherited variants and preventable exposures all change how often those changes happen. This film is general education, not medical advice, diagnosis or a guide to treatment. If you are worried about symptoms or your risk, talk to a doctor. All interactive models are schematic and all images are AI-generated. Sources: [Irish Examiner / The Guardian: cancer rates rising more quickly among younger people, WCRF analysis (6 Oct 2026)](https://www.irishexaminer.com/world/arid-41920237.html); [Tasnim News: cancer rates rising faster among younger people, international study finds (6 Oct 2026)](https://www.tasnimnews.ir/en/news/2026/10/06/3716317/cancer-rates-rising-faster-among-younger-people-international-study-finds/amp); [NCI SEER Training: what is cancer?](https://training.seer.cancer.gov/disease/cancer/); [Medical News Today: how many cells are in the human body? (Sender, Fuchs & Milo, 2016)](https://www.medicalnewstoday.com/articles/318342); [Wikipedia: Apoptosis](https://en.wikipedia.org/wiki/Apoptosis); [National Cancer Institute: the genetics of cancer](https://www.cancer.gov/about-cancer/causes-prevention/genetics); [US National Library of Medicine: retroviruses and the genetic origins of cancer, 1970–1993](https://mhm.nlm.nih.gov/spotlight/mv/feature/oncogenes); [Nobel Prize in Physiology or Medicine 1989](https://www.nobelprize.org/prizes/medicine/1989/summary/); [Wikipedia: Two-hit hypothesis](https://en.wikipedia.org/wiki/Two-hit_hypothesis); [HHMI BioInteractive: the p53 gene and cancer](https://media.hhmi.org/biointeractive/click/p53/01.html); [Review (PMC9924026): genetic progression of colorectal cancer](https://pmc.ncbi.nlm.nih.gov/articles/PMC9924026/); [Cancer Research UK: age, the forgotten cancer risk factor (2023)](https://news.cancerresearchuk.org/2023/05/29/age-the-forgotten-cancer-risk-factor/); [Wikipedia: Hayflick limit](https://en.wikipedia.org/wiki/Hayflick_limit); [PBS NOVA: cancer warrior Judah Folkman](https://www.pbs.org/wgbh/nova/article/folkman-cancer); [Cedars-Sinai: overview of cancer (spread through blood and lymph; naming by primary site)](https://www.cedars-sinai.org/health-topics/overview-of-cancer); [MedlinePlus Genetics: TP53 gene](https://medlineplus.gov/genetics/gene/tp53); [AACR: updated hallmarks of cancer (2022)](https://www.aacr.org/blog/2022/01/21/new-dimensions-in-cancer-biology-updated-hallmarks-of-cancer-published/); [UICC: GLOBOCAN 2022 global cancer data](https://www.uicc.org/news/globocan-2022-latest-global-cancer-data-shows-rising-incidence-and-stark-inequities); [WHO / IARC: four in ten cancer cases could be prevented globally (3 Feb 2026)](https://who.int/news/item/03-02-2026-four-in-ten-cancer-cases-could-be-prevented-globally)