Genes that trigger cancer could be turned off - before people are even born, according to new research.
Scientists have found a tumour 'switch' that develops hours after fertilisation.
The discovery offers hope of a screening program, personalised vaccines - or even embryo engineering.
Co author Professor Tony Perry, of the University of Bath, said: "Our work could open a new clinical chapter for the early detection of cancer."
In experiments on mice, the international team found gene activity in embryos kicks off within four hours of sperm injection.
These include 'oncogenes' which have the potential to cause cancer - if mutated. The findings are expected to apply to humans.
Prof Perry said: "Many factors responsible for the dawn of gene activity in embryos have long been known to be major oncogenes."
It is the first time a pre-set order of events has been established in one-cell embryos in any species.
Added Prof Perry: "Quite possibly, carcinogenesis recapitulates embryogenesis."
The study combined a state-of-the-art method to inject sperm into eggs with the latest techniques in messenger RNA (mRNA) sequencing.
These are chemicals that carry genetic code from DNA to a cell's protein-making machinery.
Some experts say mRNA vaccines will one day make us 'superhuman'. They have already played a key role in fighting Covid-19.
The microscopic molecule is produced in eggs before fertilisation and in embryos when the genome has been switched on.
Prof Perry and colleagues were able to differentiate between the two and characterise the 'on' switch - which was also associated with cancer.
It is inherited from eggs. Applying inhibitors stopped embryos growing almost immediately.
The researchers specifically targeted a protein called - expressed in over 70 percent of human cancers.
Blocking it turned off the switch - potentially preventing future tumours.
It is believed c-Myc and other cancer genes are dormant in eggs until they are themselves activated by fertilisation.
The work backs recent research by the same group showing gene activity in human embryos also starts at the one-cell stage.
Lead author Dr Maki Asami, also from Bath, said: "Many genes switched on from the get-go in mouse and human one-cell embryos are counterparts.
"The involvement of the same oncogenic transcription factors is predicted in both species."
It could be a game-changer in combating cancer - the causes of which remain elusive in most cases, said Prof Perry.
They also illuminate the mechanisms that regulate the start of mammalian development.
Parallels between embryos and cancer could be exploited in future to close gaps in our understanding of both. The study is in Cell Reports.
