Currently, little is known about the baseline burden or the clonal dynamics of cancer driver mutations in the normal human colon. Here, the authors employ targeted amplicon sequencing, computational modeling and spatial transcriptomics to characterize the prevalence, behavior and evolutionary fate of cancer driver mutant clones in the normal human colon, allowing a reassessment of the origins of colorectal cancer.
- Nefeli Skoufou-Papoutsaki
- Richard Kemp
- David S. Tourigny