Scientists traced leukemia back through decades of stored blood and found the first mutation usually appeared before age 20, more than 50 years before diagnosis
Acute myeloid leukemia is an aggressive blood cancer, and only about one in six people diagnosed with it survive five years. Researchers at the University of Cambridge and University College London used a rare resource: yearly blood samples from about 50,000 women in an ovarian cancer screening trial. They studied 47 women who later developed the leukemia and 46 who did not, tracing how mutations in their blood cells arose and grew over time.
In two-thirds of the women who developed leukemia, the first cancer-driving mutation had appeared before age 20, more than 50 years before diagnosis. The women were diagnosed at an average age of 72.
After that first mutation, the affected cells grew slowly for decades, taking years to double in number. Each new mutation sped things up two- to threefold, and cells carrying four cancer-driving mutations doubled in a matter of weeks.
“Serial blood samples are a fossil record of the blood’s evolution,” said Jamie Blundell of Cambridge’s Early Cancer Institute, who led the study. “They let us go back in time and reconstruct when each mutation arose and how fast it grew. What surprised us most is how predictable the growth of these clones is.”
That predictability is the key. Once a group of mutated cells, called a clone, became established, it expanded at a steady rate, slowing only when it ran out of room or was overtaken by a faster one. In principle, a clone’s growth measured from a few blood samples today could show how large it may become years later.
Many healthy older people carry blood cells with leukemia-type mutations, a condition called clonal hematopoiesis, but only a small share ever develop leukemia. Until now, no one had tracked the process year by year in the run-up to diagnosis, so it was unclear how to tell who is at real risk.
The second finding is a warning sign doctors may be missing. In at least a third of the leukemia cases, one clone had taken over most of the blood years before diagnosis, an event the researchers call a somatic sweep. None of the women who stayed cancer-free had one. The team confirmed in UK Biobank data that people with these sweeps had a greatly increased risk of leukemia, and noted that standard genetic tests often mistake such mutations for inherited ones.
“Because the growth is exponential, even modestly slowing a high-risk clone over the decade or more before diagnosis could substantially reduce the chance it becomes leukaemia,” Blundell said. That is the team’s next step: testing whether preventive treatment can slow these clones safely. Other early-stage approaches are being tested too, including a vitamin C trial in people with pre-leukemic blood disorders.
For most people, the findings are not a reason to worry. Carrying a mutation does not mean leukemia will follow, and there is no routine test to look for these clones yet. People already diagnosed with clonal hematopoiesis can ask their doctor about monitoring.
There are limits to what this shows. The study included 47 women who developed leukemia, all from one UK screening trial, and no men. In about one in five cases, the mutated cells were only detectable one to two years before diagnosis, so some cases may give little warning. The research was largely funded by UK Research and Innovation and Cancer Research UK.
Source
Watson CJ, et al. “Evolutionary dynamics in the years preceding acute myeloid leukaemia.” Nature, 2026.
DOI: 10.1038/s41586-026-11269-x
