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Clonal expansions in dividing tissues appear as a tapestry with increasing age in humans; this is most visible in blood as clonal hematopoiesis (CH). CH, associated with aging-related phenotypes and cancer risk, is frequently caused by somatic mutations in a group of known genes. Most clones, though, don’t have identified drivers.
In a new study, scientists from the Wellcome Sanger Institute, Calico Life Sciences, California, and the University of Cambridge have discovered 17 additional genes that drive the abnormal overgrowth of mutated blood cells as we age. The research provides crucial new information on the genetics behind clonal hemopoiesis, a process linked to aging and a higher risk of blood malignancies.
Scientists examined sequencing data from the UK Biobank cohort, which included over 200,000 people. They looked for genes exhibiting “positive selection” signals, which occur when mutations cause mutant cell populations to grow significantly over time.
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