Clonal haematopoiesis and ionizing radiation: risks for hematological malignancies and somatic diseases

Introduction . The influence of radiation-induced genetic instability on the formation of clonal expansion is a relevant problem in health monitoring and preventive diagnostics of oncohematological and somatic pathology in individuals exposed to long-term low-dose anthropogenic irradiation, such as nuclear industry workers and radiation diagnostics doctors. Objective . Identification of possible application points of preventive diagnostics of genome instability markers and clonal hematopoiesis in groups of individuals exposed to long-term low-dose anthropogenic irradiation. Results and discussion . Genetic instability in genes of epigenetic regulation ( DNMT3A, TET2, ASXL1 ), signaling pathways and cell proliferation ( JAK2, FLT3 ), DNA repair regulators ( TP53, PPM1D ), RNA splicing factors ( SF3B1, SRSF2 ) most often initiates clonal hematopoiesis, which is realized more frequently by myeloid and less frequently by lymphoid neoplasia. The influence of clonal hematopoiesis on the development of somatic diseases is mediated by the combined effect of carrying these mutations and the processes of chronic inflammation. Low-dose ionizing radiation is capable of initiating clonal expansion mainly due to mutations in DNMT3A and TET2 genes. There is a lack of studies on the assessment of increased morbidity against the background of clonal hematopoiesis in groups of occupational risk of low-dose ionizing radiation exposure (workers in the nuclear industry and doctors of radiation diagnostics), which requires further study. Conclusions . Studies aimed at identifying risk markers of morbidity growth in the setting of clonal hematopoiesis in groups of workers exposed to long-term anthropogenic action of low-dose ionizing radiation form the basis for developing cohort-oriented programs of disease prevention in these individuals.