Written by a parent, not a doctor. Nothing here is medical advice.

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Myth Verdict: Partly true

“Nobody knows where childhood cancer comes from”

Updated September 2026. Citations at bottom of page.

Also known as: causes, why, inherited, genetic, environment, did I cause it, vaccines, power lines, daycare, breastfeeding, prenatal origin

Partly true. For most children with leukemia, nobody can say why it happened, and that is the honest answer. But for the common form of childhood B-ALL, researchers have worked out a surprising amount about how it starts: in many kids the first step happens before birth, most who take that step never get sick, and a second push in early childhood is needed. Here is that story in plain terms, then the everyday things people ask about.

The short version

For most children with leukemia, nobody can say why it happened, and that is the honest answer. The National Cancer Institute says the cause of the cell changes in childhood ALL is usually unknown, and the American Cancer Society says most children with leukemia have no known risk factor at all.1, 2, 3

But “nobody knows where it comes from” is only half right. For the common form of childhood B-ALL, researchers have worked out a surprising amount about how it starts. In many kids the first step happens before birth. Most babies who take that first step never get leukemia. A second push in early childhood is usually needed, and there is a well-supported idea, not yet proven, about what that push is.5, 19, 22, 47 That is why I call this one partly true.

This page has three parts: how the disease is thought to start, the everyday things people ask about, and what “genetic” does and does not mean.

Part 1: How B-ALL starts, according to Mel Greaves

Most of what is known here comes from one research group, led by Mel Greaves in London, working over about thirty years.45, 47, 48, 5 His model, in plain words, makes three claims. I will take them one at a time, with the evidence for each and why it matters.

Claim 1: The first change happens before birth

The evidence started with twins. In 1998, Greaves’ group studied a pair of identical twins who both got B-ALL, one at three and a half, the other at nearly five. Their leukemia cells carried the same fused gene, ETV6::RUNX1, broken and joined at exactly the same point in the DNA.18 Why does that matter? Because this fusion is an accident that happens once, in one cell. Every time it happens, the DNA breaks in a slightly different place, the way a tear in a sheet of paper is never quite the same twice. Two children with a tear in exactly the same place did not each have the accident; one of them had it, and the cells crossed to the other. Identical twins share a placenta, so the only time that could have happened is before birth.18, 48 Doctors had noticed since 1882 that when one identical twin gets leukemia as a baby the other often does too; this was the explanation.48

Then came the heel-prick cards. Every newborn gets a drop of blood taken from the heel, and the cards are stored for years. In 1997, Greaves’ group went back to the cards of three babies who had developed an infant leukemia (the KMT2A kind, then called MLL) at five months, six months and two years old, and found each child’s specific leukemia fusion already on the card from the day they were born.46 In 1999 they did the same for the common childhood kind: of nine usable cards from British and Italian children who got ETV6::RUNX1 leukemia at ages two to five, six already carried that child’s fusion at birth.19 A Michigan group found the leukemia’s genetic fingerprint on the newborn cards of 12 of 17 children, including every child whose leukemia had extra chromosomes, and an Austrian case placed that chromosome gain before birth too.20, 21

What this means for a parent is the part I found genuinely steadying. In these children, the change was in the blood on the day they were born, before daycare, before food, before anything that happened at home. The clock had already started.

Claim 2: The first change is not the disease

If the fusion were enough on its own, every baby born with it would get leukemia. They don’t. In 2008 Greaves’ group found a pair of identical twins where one had leukemia and the other was healthy, and the healthy twin’s blood carried a small population of cells with the same fusion, sitting there doing no harm at the time they were studied.50 That is what the first change makes: not leukemia, but a pre-leukemia cell that can survive and wait.

The cord-blood screening studies say the same thing on a bigger scale.

Cord-blood screening of healthy newborns

Of 100 newborns, between 1 and 5 already carry the ETV6::RUNX1 change

6 of 567healthy cord-blood samples carried the fusion in a 2002 UK study, about 1 in 100 (the dark dot)
50 of 1,000screened positive with a more sensitive DNA test in a 2018 Danish study, 5 in 100 (all five dots)

Two studies, two methods, two samples; the true share is somewhere around there, not a measured range. Neither study followed the babies forward. Sources 22 and 23.

When researchers tested cord blood from healthy newborns for this fusion, a 2002 UK study found it in 6 of 567 samples, about 1 in 100, and a 2018 Danish study with a more sensitive DNA test found it in 50 of 1,000, 5 in 100.22, 23 Childhood leukemia of any kind, by contrast, is diagnosed in about 5 children per 100,000 per year.38 The UK team put the comparison in their own paper: the fusion is roughly 100 times more common in newborns than the leukemia it goes with.22 Greaves’ estimate from the same arithmetic is that around 1 in 100 of these silent clones ever becomes leukemia, and about 99 in 100 never do.5 A 2025 Barcelona study found the fusion in 48 of 741 cord-blood samples, 6.5 percent, and asked whether anything in pregnancy moved that number; its endpoint was the marker at birth, not leukemia, and it cannot say what any of those babies went on to.24 None of these studies followed the babies forward, so Greaves’ figure is an estimate from comparing two frequencies, not a measurement in followed children, and it says nothing about any one child. But the gap is wide however you draw it.

So the first change is common, the disease is rare, and something else has to happen in between.

Claim 3: A second push in early childhood, and what Greaves thinks pushes it

Greaves first proposed his answer in 1988 and has been testing it since.45, 49, 5 In plain terms: a child’s immune system needs practice in the first year or two of life, and gets it from ordinary germs. In a child who already carries the silent clone from before birth, an ordinary infection that arrives later than it would have in earlier generations can set off an immune reaction that lands the second change in one of those waiting cells. He calls it the delayed-infection hypothesis.

Two things to be clear about. He is not pointing at one virus or one germ. The idea is about common childhood infections in general and, above all, their timing.5, 49 And it is not that leukemia is caught. It is that when a child’s immune system first meets everyday illness may decide whether a silent clone ever wakes up.

Why take the idea seriously? Because it explains things the older ideas did not. This form of leukemia peaks at ages two to five, mostly in wealthier countries. Across many populations it is rarer in children who went to daycare early, were breastfed longer or had older siblings, all of which mean meeting ordinary germs sooner.33, 34, 5 And in 2026 a UK lab tested the timing part directly in mice engineered to carry ETV6::RUNX1: moved from a clean facility into a germ-rich one after weaning, 6 of 54 developed leukemia; raised in the germ-rich setting from birth, 0 of 400 did.37

Why not call it settled? Because the human evidence is patterns across populations plus animal experiments, not the trigger observed in an individual child, and the studies of actual infections are messy: when UK researchers used medical records instead of memory, children who later got ALL had more recorded infections in their first year, not fewer, and a second record-based study found no protective effect at all.35, 36 Being around other children, catching something, seeing a doctor and building a particular immune response are four different things, and the studies measure them differently.

Here is the whole model as one child’s path.

How common B-ALL comes to be

One child's path, in four steps

This is the two-step picture that Mel Greaves and colleagues built up from twins, newborn blood spots and population studies. It is drawn for the ETV6::RUNX1 form of common early-childhood B-ALL, as one illustrative child. The cell counts are illustrative, not measured. Press play and read the steps as they light up.

Before birth Birth Early childhood Usually ages 2 to 5 developing white-blood cells 1 · first change (e.g. ETV6::RUNX1) 2 · a small, silent clone roughly 1 in 100 newborns 3 · for most, nothing more the clone stays quiet (about 99 in 100, an estimate) 4 · for a few, a second change proposed trigger: an ordinary infection, years later the clone takes off: leukemia this form peaks at ages 2 to 5
About 14 seconds. Each step lights up below as it happens.
  1. Before birth. Somewhere in the developing blood, one white-blood-cell precursor picks up a change. In the form drawn here it is two genes fused together, ETV6::RUNX1; in others it is extra copies of several chromosomes. This is the “first hit.” In the children studied it happened in the womb, before anything a parent could do or not do.
  2. At birth. That cell has made a small crowd of copies, but they are not leukemia. They sit quietly among normal cells. A UK screening study found the fusion in 6 of 567 healthy cord-blood samples, roughly 1 in 100; a Danish study with a more sensitive DNA test found it in 50 of 1,000.
  3. Early childhood, most kids. For most children who carry the clone, that is the end of the story. Greaves estimates about 99 in 100 never progress, by comparing how common the marker is with how common the leukemia is. The studies did not follow individual babies, so nobody can say whether a given clone persists or disappears; the drawing keeps it visible and quiet.
  4. Early childhood, a few kids. In a small share of carriers, a second change lands in one of the clone's cells and it can grow without limit. Greaves' proposed trigger is the immune system's response to an ordinary infection, met later in life than it would have been a century ago. That part is a well-supported hypothesis, backed by population patterns and mouse experiments, not a proven event in any one child. This form of leukemia peaks at ages 2 to 5.

Not every childhood leukemia follows this path. Infant leukemia with a KMT2A (MLL) fusion also starts before birth; Greaves describes it as essentially completed in the womb, and it appears before age 1. T-cell ALL and the rarer B-ALL subtypes have their own routes, less well mapped. Sources 5, 22, 23, 46, 48 and 50.

The animation is drawn for the ETV6::RUNX1 form of common B-ALL, as one illustrative child. Steps 3 and 4 are alternatives, not stages every child passes through, and the rough odds on it, about 1 in 100 newborns carrying the clone and about 1 in 100 of those progressing, are the screening result and Greaves’ estimate rather than measurements in followed children.5, 22, 23

Which leukemias this fits

The model is built for the common B-ALL of early childhood, the ETV6::RUNX1 and extra-chromosome forms.5 Infant leukemia with a KMT2A fusion also starts before birth, but Greaves describes it as essentially complete in the womb, with no second step needed; it appears before age one and identical twins nearly always both get it.5, 46, 48 T-cell ALL and the rarer B-ALL subtypes have their own routes, less well mapped.5, 47

Part 2: The everyday things people ask about

The questions below come up in every parent group I have been in. The studies that answer them report a ratio: how often leukemia turned up in children with the exposure compared with children without it. A ratio of 1.0 means no difference. Below 1.0 means fewer cases in the exposed group; above it, more. The line through each dot is the 95 percent confidence interval, the range of ratios the data fit reasonably well. A pattern across a population is not a cause in one child, and most of these studies rest on parents remembering the past after a diagnosis, which is a weaker kind of evidence than records made before anyone was sick.

Vaccines

Two Danish studies followed every child born in the country, linking vaccination records to cancer records, so nothing depended on memory.6, 7

Vaccines · two Danish register studies

Leukemia among vaccinated children compared with unvaccinated, and per extra dose

Each dot compares children with the exposure against children without it. 1.0 means leukemia turned up at the same rate in both groups.

Hazard ratios with 95% confidence intervals, from national vaccination and cancer records made before any child was sick. Sources 6 and 7.

Both dots sit on the 1.0 line. The 2017 study, 1.2 million children born 1990 to 2008, found a ratio of 1.01 for the MMR vaccine and nothing convincing for any vaccine it looked at.6 The 2025 study, 1.4 million children born 1997 to 2018, found 1.01 per additional dose, with a line so narrow it barely shows.7 The same study’s comparison of any vaccination against none came out at 2.76 with a huge range, 0.66 to 11.58, because so few unvaccinated children get leukemia that the comparison cannot settle anything either way.7 What I take from the two studies together: across 2.6 million children, vaccines did not move the leukemia rate.

Food, including what a mother ate in pregnancy

There is no established dietary cause of childhood leukemia. A 2025 review pulled together studies of processed meat, vegetables, fruit and coffee and found associations in both directions, all from families remembering meals after a diagnosis, none strong enough to name a food.8 A pooled international study found slightly fewer cases among mothers who reported taking folic acid or vitamins in pregnancy.9 None of it can connect a particular meal, or a missed vitamin, to a particular child.

Stress

The largest studies looked at something far heavier than everyday worry. One followed six million Danish and Swedish births and asked whether mothers who lost a close family member in the year before or during pregnancy had children with more cancer. Overall they did not, though a few rare cancer types showed signals the authors thought worth more study.10 A second study, of children who themselves lost a close relative before age 15, found a small increase in childhood cancer overall, a ratio of 1.10, and the authors could not say whether stress itself was the reason.11 Neither study looked at ordinary stress: a hard pregnancy, arguments, a demanding job. Nothing has shown those cause B-ALL.

Household products

This one I will not call closed, because it is not. Pooled studies that asked parents about pesticide use at home, and about painting during certain windows, found somewhat more cases among the exposed children.12, 13 Those studies leaned on memory after diagnosis, families used different products, and ordinary cleaning products were not the categories studied. It is a lead for researchers, not a finding about any particular house.

Phones and wireless, and power lines

A 2024 systematic review found moderate-certainty evidence that living near transmitters, the towers and base stations, likely does not raise childhood leukemia risk; the handset research is mostly about brain tumors, not leukemia, and this is a different kind of energy from an X-ray.14, 15 Power lines are a separate question about very low-frequency magnetic fields. Older studies sometimes linked the strongest household fields with childhood leukemia; a pooled analysis of newer studies did not find it, a broader review kept some high-exposure associations, and the NCI calls the question unresolved, partly because so few children have the highest exposures.16, 17, 15 Not an established cause, and not fully closed.

Daycare, breastfeeding and siblings

These are the patterns that led Greaves to his idea, so they belong here rather than with the worries above.

Early-life exposure · studies that asked parents to remember

ALL among children who went to daycare early or were breastfed longer, compared with children who did not

Dots below 1.0 mean fewer cases of ALL were seen in the exposed group. All three come from parents remembering after a diagnosis, so read them as patterns, not proof.

Odds ratios with 95% confidence intervals. The UK study is one of the eleven inside the pooled study, so the third row is not an independent confirmation of the second. Sources 33 and 34.

All three dots sit below 1.0. In a pooled study of 7,399 children with ALL across eight countries, children who had been breastfed for six months or more had a ratio of 0.86, and children who went to a daycare center in their first year had 0.77.33 The UK study that started this line of research found 0.48 for formal daycare in infancy, against children with no regular social activity outside the family at all.34 The UK study is one of the eleven inside the pooled study, so the third row is the same signal seen up close, not a separate confirmation.

A 2024 Danish study is worth singling out because it did not depend on memory: it used feeding records made before any child was sick, for 309,473 children, and found a ratio of 0.62 for exclusive breastfeeding of three months or more. It rests on only 74 cases, so its range runs from 0.39 almost to 1.0.32 Birth order, the older-sibling version of the same idea, came out weak and inconsistent in the pooled study and showed no clear link in the UK one.33, 34

What all this means: the pattern Greaves’ idea predicts is there, in several countries, for daycare and for breastfeeding. What it does not mean is that any of this is a recipe. Nothing here shows that a different childcare or feeding decision would have changed what happened to a particular child, and the research does not say that.32, 33, 34, 37

Radiation

Ionizing radiation, the kind in X-rays and CT scans, is the one outside cause that is firmly established. It has been known since 113,011 survivors of Hiroshima and Nagasaki were followed from 1950 to 2001 and leukemia rose with the dose they received.28 The NCI lists X-rays in pregnancy and radiation after birth among the recognized risk factors for childhood ALL.3

CT scans · nine European countries, published 2023

How much extra risk a CT scan adds, in the study's own units

1 to 2 in 10,000extra blood cancers over the following 12 years, for every 10,000 children scanned at a typical marrow dose of about 8 milligray. The study assembled 948,174 people scanned before age 22 and analyzed 876,771 of them.

A modeled estimate from the dose-response the study observed, for blood cancers of all kinds, not B-ALL alone. Source 29.

The European study behind that number followed 876,771 people who had a CT scan before age 22 and found blood cancers rose with the estimated dose to bone marrow. For a typical scan, the modeled extra risk works out to one or two extra blood cancers among every 10,000 children scanned, over the following 12 years.29 A 2025 study of 3.7 million children in the US and Ontario put it a different way: by its model, about 10 percent of the blood cancers in that group, with a range of 5.8 to 14.2 percent, could be attributed to medical imaging.30 Both are model estimates for blood cancers of all kinds, and children who get scanned are often already sick, which muddies the picture. An ordinary X-ray delivers far less than a CT, and a needed scan usually has benefits that outweigh this.31 None of it can say that one scan caused one child’s leukemia.

Part 3: “Genetic” is not the same as “inherited”

Your child’s leukemia report will list gene changes, and it is natural to read them as something passed down. Most are not. A change found only in the leukemia cells arose in those cells, as in Claim 1 above. An inherited predisposition means a change in the DNA the child was born with, present in the body’s cells generally (sometimes only some of them), and that is a different and much rarer thing. It can come from a parent or can appear new in that child.25, 26, 41

Two sequencing studies

How many children with leukemia carried a cancer-predisposing change in the DNA they were born with

2.8%47 of 1,703 children and young adults with ALL, 2022, St. Jude and COG research samples
8.5%95 of 1,120 children across many cancer types, 2015, St. Jude, including cancers that run in families4.4% in the leukemia part of that group: 26 of 588 with ALL or AML

Different groups of children and different gene lists, so these are two answers, not one. A change present from birth can be inherited from a parent or can arise new in the child. Sources 25 and 26.

When researchers sequenced the inherited DNA of 1,703 children and young adults with ALL, 47 carried a change known to raise cancer risk, 2.8 percent.25 A 2015 study across many childhood cancers found 8.5 percent overall, higher because it included cancer types that run in families, and 4.4 percent in its leukemia group.26 The two studies tested different children and different genes, so they are two answers rather than one, and carrying a variant does not prove it explains that child’s leukemia. Still, the shape is clear: for the large majority of children with leukemia, there is no inherited predisposition to find.

The conditions that do raise leukemia risk are real, and your team screens for them: Down syndrome, Li-Fraumeni syndrome, constitutional mismatch repair deficiency, and rare inherited changes in genes such as ETV6, PAX5 and IKZF1.4 Down syndrome shows what a strong predisposition looks like: in a cohort of 3.9 million children, about 1.7 percent of those with Down syndrome developed ALL by age 14, against 0.066 percent of those without.27 The questions worth asking your team are whether the changes on the report were found only in the leukemia cells, whether testing of your child’s own DNA was done, and whether a genetic counselor would be useful for the rest of the family.

How rare it is

In the United States, childhood leukemia of all types is diagnosed in about 4.9 of every 100,000 children and teenagers per year, and the rate has been rising by about 0.6 percent a year since 2014.38 An international registry study covering 62 countries found 4.64 per 100,000 for children under 15 between 2001 and 2010.39, 40 A rising rate is an observation; it does not point at any particular modern exposure, and there is no honest single number for the share of childhood leukemia explained by known causes, because the estimates above answer different questions and cannot be added up.25, 26, 30

Other childhood cancers, briefly

“Childhood cancer” is many diseases, and for some the origins are better understood than people think. Retinoblastoma usually comes down to changes in one gene, RB1, whether inherited or arising in the eye.41 Wilms tumor and neuroblastoma grow out of tissue that was still developing, with rare familial forms.42, 43 A lymphoma common in equatorial Africa, endemic Burkitt, has clear links to the Epstein-Barr virus and malaria.44 For many diagnoses, “we cannot explain why this child” remains fair. “We know nothing about where it comes from” does not.

What I take from this

Two different questions hide inside “where does it come from.” How does the disease develop? For common childhood B-ALL, we know a good deal: a first change before birth, a silent clone that usually goes nowhere, a second push in early childhood that Greaves ties to the timing of ordinary infections. Why did it develop in this child? That, almost always, nobody can answer, and the research does not pretend to.1, 3, 5

What I would carry out of this page is the part that is settled: in the children who have been studied, the first step was taken before they were born.

Where I read this

  1. National Cancer Institute. Support for Families: Childhood Cancer. Accessed September 23, 2026. Page. Where: NCI guide, discussion of why children get cancer.
  2. American Cancer Society. Causes, Risk Factors, and Prevention of Childhood Leukemia. Accessed September 23, 2026. Page. Where: Most affected children have no known risk factor; known risk factors explain few cases.
  3. National Cancer Institute. Childhood Acute Lymphoblastic Leukemia Treatment (PDQ), patient version. Accessed September 23, 2026. Page. Where: Risk Factors section: the cause of childhood ALL cell changes is often unknown; recognized risk factors.
  4. National Cancer Institute. Childhood Acute Lymphoblastic Leukemia Treatment (PDQ), health professional version. Accessed September 23, 2026. Page. Where: “Genetic predisposition” and “Risk factors” (Down syndrome, Li-Fraumeni, constitutional mismatch repair deficiency, germline ETV6/PAX5/IKZF1, radiation).
  5. Greaves M. A causal mechanism for childhood acute lymphoblastic leukaemia. Nature Reviews Cancer 2018. free full text (PMC). Where: Abstract for the two-step model. The approximately 99% nonprogression estimate requires the full-text section on the frequency of prenatal initiation, rather than the abstract.
  6. Søegaard SH, et al. Childhood vaccinations and risk of acute lymphoblastic leukaemia in children. International Journal of Epidemiology 2017. PubMed. Where: Abstract, Methods and Results: 1,225,404 Danish births, 1990–2008; follow-up to age 15 or end of 2009; vaccinated versus unvaccinated comparison; 490 ALL cases; MMR hazard ratio 1.01 (95% CI 0.76–1.34).
  7. Alberts A, et al. Childhood vaccinations and the risk of leukemia: a nationwide cohort study. International Journal of Cancer 2025. PubMed. Authors’ institutional abstract. Where: Abstract, Methods, Results, and concluding limitation: birth cohort 1997–2018; per-dose ALL hazard ratio 1.01 (95% CI 0.96–1.05); any vaccine versus none 2.76 (0.66–11.58); few unvaccinated cases.
  8. Flores-García MK, et al. Maternal and infant diet play a role in acute leukemia development: an expanded systematic review and meta-analysis. Clinical Nutrition ESPEN 2025. PubMed. Where: Observational studies searched through April 2022; associations in both directions, all from recalled diet.
  9. Metayer C, et al. Maternal supplementation with folic acid and other vitamins and risk of leukemia in offspring: a Childhood Leukemia International Consortium study. Epidemiology 2014. PubMed. Where: Pooled case-control data 1980 to 2012; inverse association with reported supplement use.
  10. Li J, et al. Antenatal maternal bereavement and childhood cancer in the offspring: a population-based cohort study in 6 million children. British Journal of Cancer 2012. free full text (PMC). Where: Abstract, Materials and Methods, and Results: maternal bereavement during the year before or during pregnancy; 2,743,560 Danish and 3,400,212 Swedish births; no clear overall cancer association, with subtype findings.
  11. Momen NC, et al. Early life bereavement and childhood cancer: a nationwide follow-up study in two countries. BMJ Open 2013. PubMed. Free full text (PMC). Where: Abstract, Participants and Results; Materials and Methods, Study participants and follow-up; Discussion: bereavement before age 15, not maternal pregnancy stress; overall childhood-cancer HR 1.10 (95% CI 1.04–1.17); causal interpretation uncertain.
  12. Bailey HD, et al. Home pesticide exposures and risk of childhood leukemia: findings from the Childhood Leukemia International Consortium. International Journal of Cancer 2015. free manuscript (PMC). Where: Pooled retrospective case-control studies from North America, Europe and Australasia; positive associations with recalled home pesticide use.
  13. Bailey HD, et al. Home paint exposures and risk of childhood acute lymphoblastic leukemia: findings from the Childhood Leukemia International Consortium. Cancer Causes & Control 2015. free manuscript (PMC). Where: Retrospective studies in six countries; associations depended on the exposure window.
  14. Karipidis K, et al. The effect of exposure to radiofrequency fields on cancer risk in the general and working population: a systematic review of human observational studies, Part I. Environment International 2024. PubMed. Where: Studies published 1994 to 2022; moderate-certainty evidence that fixed-site transmitters likely do not increase childhood leukemia risk.
  15. National Cancer Institute. Electromagnetic Fields and Cancer. Accessed September 23, 2026. Fact sheet. Where: Sections on non-ionizing fields, power-line exposures and childhood cancer, and cell-phone base stations; high-exposure estimates are difficult to interpret.
  16. Amoon AT, et al. Pooled analysis of recent studies of magnetic fields and childhood leukemia. Environmental Research 2022. PubMed. Where: No association in the recent pooled case-control studies.
  17. Brabant C, et al. Exposure to magnetic fields and childhood leukemia: a systematic review and meta-analysis of case-control and cohort studies. Reviews on Environmental Health 2023 (online 2022). PubMed. Where: Retained some positive high-exposure associations.
  18. Ford AM, et al. Fetal origins of the TEL-AML1 fusion gene in identical twins with leukemia. Proceedings of the National Academy of Sciences 1998. PubMed. Where: Abstract: identical twins diagnosed at 3 years 6 months and 4 years 10 months shared one unique, non-inherited TEL-AML1 fusion sequence and an identical rearranged IGH allele; the authors' explanation is a single-cell origin in one fetus with spread to the other through the placenta. A molecular case study, not a survey.
  19. Wiemels JL, et al. Prenatal origin of acute lymphoblastic leukaemia in children. The Lancet 1999. PubMed. Where: Abstract, Methods and Findings: 12 singleton cases plus a twin pair, both twins diagnosed at age four; three singleton cards unsuitable; six of nine evaluable singleton spots positive; negative spots are uninformative about timing.
  20. Taub JW, et al. High frequency of leukemic clones in newborn screening blood samples of children with B-precursor acute lymphoblastic leukemia. Blood 2002. Publisher. Article abstract. Where: Abstract, patient-specific IgH testing and results: 12 of 17 newborn cards positive, including all six hyperdiploid cases. The marker was a matching IgH rearrangement, not a chromosome count. Abstract opened; full article not retrieved.
  21. Panzer-Grümayer ER, et al. Nondisjunction of chromosomes leading to hyperdiploid childhood B-cell precursor acute lymphoblastic leukemia is an early event during leukemogenesis. Blood 2002. PubMed. Where: Austrian case study placing the chromosome-gain event before birth.
  22. Mori H, et al. Chromosome translocations and covert leukemic clones are generated during normal fetal development. Proceedings of the National Academy of Sciences 2002. free full text (PMC). Where: Abstract, Materials and Methods, and Results: six of 567 cord-blood samples positive for TEL-AML1/ETV6::RUNX1; fusion frequency compared with disease frequency (the abstract puts the fusion at a frequency about 100-fold greater than the risk of the corresponding leukemia), not prospective progression measured in these newborns.
  23. Schäfer D, et al. Five percent of healthy newborns have an ETV6-RUNX1 fusion as revealed by DNA-based GIPFEL screening. Blood 2018. free full text (PMC). Where: Results and Discussion: 50 of 1,000 anonymous Danish cord-blood samples positive using GIPFEL; no individual cancer follow-up; the result is not a confidence interval around the 2002 estimate.
  24. Benítez L, et al. Modulation of the ETV6::RUNX1 gene fusion prevalence in newborns by corticosteroid use during pregnancy. International Journal of Molecular Sciences 2025. PubMed. Full text. Where: Abstract and Sections 2 and 4: 48 of 741 positive samples (6.5%) within the IMPACT-BCN trial; usual care, Mediterranean diet and mindfulness groups were randomized; corticosteroid exposure was observational; endpoint was fusion detection, not leukemia incidence.
  25. Brady SW, et al. The genomic landscape of pediatric acute lymphoblastic leukemia. Nature Genetics 2022. free manuscript (PMC). Where: St. Jude and COG trial samples; 47 of 1,703 germline-sequenced participants (2.8 percent) carried pathogenic or likely pathogenic predisposition variants.
  26. Zhang J, et al. Germline mutations in predisposition genes in pediatric cancer. New England Journal of Medicine 2015. Publisher. Abstract and figure legends. Where: Abstract, Methods and Results for 95 of 1,120 (8.5%); Figure 4 legend for mosaicism. The original leukemia-subset figure, 26 of 588 (4.4%), is retained pending full-text verification.
  27. Marlow EC, et al. Leukemia risk in a cohort of 3.9 million children with and without Down syndrome. The Journal of Pediatrics 2021. free manuscript (PMC). Authors’ institutional abstract. Where: Abstract for 3,905,399 children, births 1996–2016, and cumulative ALL incidence with Down syndrome, 1,714 per 100,000 at age 14. The non-Down-syndrome comparison requires the full-text cumulative-incidence results.
  28. Hsu WL, et al. The incidence of leukemia, lymphoma and multiple myeloma among atomic bomb survivors: 1950 to 2001. Radiation Research 2013. PubMed. Where: Abstract, cohort description and results: 113,011 survivors; incidence follow-up 1950–2001; dose-related leukemia risk; ages at exposure varied.
  29. Bosch de Basea M, et al. Risk of hematological malignancies from CT radiation exposure in children, adolescents and young adults. Nature Medicine 2023. Open access. Publisher-provided full text. Where: Abstract for the modeled 12-year excess at about 8 mGy marrow dose; Results, Descriptive analyses (journal page 3112), for 948,174 assembled and 876,771 analyzed; Discussion for dose uncertainty and confounding by indication.
  30. Smith-Bindman R, et al. Medical imaging and pediatric and adolescent hematologic cancer risk. New England Journal of Medicine 2025. PubMed. Authors’ institutional abstract. Where: Abstract, Methods and Results: 3,724,623 children born 1996–2016 in six US systems and Ontario; follow-up through 2017; estimated attributable fraction of hematologic cancers 10.1% (95% CI 5.8–14.2), not an individual cancer probability.
  31. National Cancer Institute. Computed Tomography (CT) Scans and Cancer. 2024. Fact sheet. Where: Sections explaining CT radiation exposure, cancer risk, and clinical benefits and risks.
  32. Søegaard SH, et al. Exclusive breastfeeding duration and risk of childhood cancers. JAMA Network Open 2024. PubMed. Where: Abstract, Design/Participants and Results: 309,473 children with available feeding records; 74 BCP-ALL cases; exclusive breastfeeding ≥3 versus <3 months, adjusted hazard ratio 0.62 (95% CI 0.39–0.99); follow-up at ages 1–14.
  33. Rudant J, et al. Childhood acute lymphoblastic leukemia and indicators of early immune stimulation: a Childhood Leukemia International Consortium study. American Journal of Epidemiology 2015. free manuscript (PMC). Publisher abstract. Author-uploaded full text. Where: Abstract for sample sizes; Table 1 (journal page 551) for the included UKCCS study; Table 3 (page 554) for breastfeeding ≥6 months versus never, OR 0.86 (95% CI 0.79–0.94), and daycare center before age one versus none before one, OR 0.77 (0.71–0.84); Discussion for recall, participation, and confounding limits.
  34. Gilham C, et al. Day care in infancy and risk of childhood acute lymphoblastic leukaemia: findings from UK case-control study. BMJ 2005. free full text (PMC). Author-repository full text. Where: Abstract and Methods for 1,286 ALL cases and 6,305 controls, diagnoses 1991–1996; Table 2, journal page 3, formal daycare OR 0.48 (95% CI 0.37–0.62) versus no social activity outside the family; Table 3 for siblings. Table 2 uses participants with available activity data.
  35. Roman E, et al. Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study. American Journal of Epidemiology 2007. PubMed. Where: Medical records for children diagnosed at 2 to 5 in 1991 to 1996: cases had more recorded first-year infections, not fewer.
  36. Cardwell CR, et al. Infections in early life and childhood leukaemia risk: a UK case-control study of general practitioner records. British Journal of Cancer 2008. free full text (PMC). Where: Children born 1987 to 2005; no protective association for recorded infant infections.
  37. Cazzaniga V, et al. Timing of microbial exposure and risk of infection-promoted acute lymphoblastic leukemia. Haematologica 2026. Open access. Full article PDF. Where: Article PDF, journal pages 3525–3526 and Figure 1: clinical ALL in 6/54 transferred mice versus 0/400 raised in the microbe-rich facility; additional subclinical findings and unequal routine subclinical screening are described in the text. First published online April 16, 2026; later issue pagination is not the online publication date.
  38. National Cancer Institute, SEER. Cancer Stat Facts: Childhood Leukemia. Accessed September 23, 2026. Page. Where: New Cases and Rate of New Cases and Deaths, and Trends in Rates: age-adjusted 4.9 per 100,000 per year, ages 0–19, diagnoses 2019–2023; average annual increase 0.6% during 2014–2023; all leukemia types.
  39. Steliarova-Foucher E, et al. International incidence of childhood cancer, 2001 to 10: a population-based registry study. The Lancet Oncology 2017. Publisher. Where: 153 registries in 62 countries; world-standardized leukemia rate 46.4 per million (4.64 per 100,000) for ages 0 to 14.
  40. International Agency for Research on Cancer. International Incidence of Childhood Cancer, Volume III. Accessed September 23, 2026. Project site. Print-release announcement. Where: IICC-3 project and official IARC release announcements: completed online volume in December 2025; print announcement April 29, 2026. The volume reports historical observations.
  41. National Cancer Institute. Childhood Cancer Genomics (PDQ), health professional version. Accessed September 23, 2026. Page. Where: Retinoblastoma section: constitutional versus tumor-restricted RB1 alterations; rare tumors without RB1 inactivation mean RB1 is not universal. Genomic findings do not by themselves establish inheritance from a parent.
  42. National Cancer Institute. Wilms Tumor and Other Childhood Kidney Tumors Treatment (PDQ), health professional version. Accessed September 23, 2026. Page. Where: Kidney precursor tissue and predisposition involving WT1 and chromosome 11p15.
  43. National Cancer Institute. Neuroblastoma Treatment (PDQ), health professional version. Accessed September 23, 2026. Page. Where: Developmental origins and rare familial forms involving ALK and PHOX2B.
  44. National Cancer Institute, Division of Cancer Epidemiology and Genetics. Burkitt Lymphoma: Overview of Research. Accessed September 23, 2026. Page. Where: Endemic Burkitt lymphoma's links to Epstein-Barr virus and malaria.
  45. Greaves MF. Speculations on the cause of childhood acute lymphoblastic leukemia. Leukemia 1988. PubMed. Where: PubMed bibliographic record: 1988, Leukemia 2(2):120–125. No abstract is provided in the opened record. The history is also described in the 2018 review; full 1988 text was not verified.
  46. Gale KB, Ford AM, Repp R, Borkhardt A, Keller C, Eden OB, Greaves MF. Backtracking leukemia to birth: identification of clonotypic gene fusion sequences in neonatal blood spots. Proceedings of the National Academy of Sciences 1997. free full text (PMC). Where: Patients, Results and Discussion: three MLL-AF4 cases diagnosed at 5, 6 and 24 months; matching fusion sequences in neonatal blood spots establish prenatal initiation, not completion of all leukemic evolution in utero.
  47. Greaves MF, Wiemels J. Origins of chromosome translocations in childhood leukaemia. Nature Reviews Cancer 2003. PubMed. Where: Abstract: chromosome translocations frequently arise prenatally and are early, usually necessary but insufficient events.
  48. Greaves MF, Maia AT, Wiemels JL, Ford AM. Leukemia in twins: lessons in natural history. Blood 2003. PubMed. Author-uploaded full text. Where: Abstract and opening historical discussion, journal page 2321 onward: first reported concordant identical infant twins in 1882; shared clonal origin and placental transfer; variable latency and additional postnatal events. Author-uploaded article text was opened.
  49. Greaves M. Infection, immune responses and the aetiology of childhood leukaemia. Nature Reviews Cancer 2006. PubMed. Where: The mid-point review of the delayed-infection hypothesis and the evidence for it at that time.
  50. Hong D, Gupta R, Ancliff P, et al. Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia. Science 2008. PubMed. Article abstract. Where: Abstract: discordant monochorionic twins, one with a pre-leukemic population and one with leukemia; experimentally altered self-renewal and survival. This is not lifetime follow-up proving that the unaffected twin never developed leukemia. Full article not retrieved.