In recent years, growing evidence linking clonal hematopoiesis (CH) to aging, inflammation, inflammation-driven systemic diseases, cardiovascular risk, and cancer has increased interest in its role in disease evolution and somatic variation.In parallel, advances in next-generation and single-cell sequencing technologies, combined with computational modeling, have significantly improved our understanding of CH biology. 123 CH was initially identified through age-related skewing of X-chromosome inactivation and later associated with somatic TET2 mutations.It is now recognized as a fundamental age-related process characterized by the expansion of hematopoietic stem and progenitor cells carrying somatic variants and mosaic chromosomal alterations (mCAs), with prevalence increasing sharply with age.
Kırkızlar et al. (Fri,) studied this question.
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