查看文章

Clonal hematopoiesis (CH) increases the risk of hematological malignancies and other adverse outcomes. The most common driver mutations occur in DNMT3A and TET2. However, it is still unclear how mutant DNMT3A and TET2 perturb human stem/progenitor cell homeostasis allowing mutant clones to expand. Studies of human CH have been limited by availability of samples from subjects without co-existing malignancy and high-precision methods for comparing mutant and wild-type (WT) cells in the same individual.