KEY POINTS
- The review examines whether disrupted circadian rhythms could act as a cofactor in radiation-induced acute myeloid leukaemia.
- Core clock genes, including BMAL1, CLOCK, PER and CRY, regulate cell-cycle checkpoints, haematopoiesis and DNA-damage responses involving ATM–CHK2 and p53 signalling.
- PER1, PER2 and PER3 are frequently downregulated in peripheral blood from patients with acute myeloid leukaemia, while radiation exposure can also alter clock-gene expression.
- Circadian disruption may enhance inflammation, immune senescence and myeloid-derived suppressor-cell accumulation while compromising repair of radiation-induced DNA damage.
- Direct in vivo evidence combining experimentally induced circadian disruption, ionizing radiation exposure and subsequent acute myeloid leukaemia development is currently absent.
CLINICAL TAKEAWAY
The proposed interaction is biologically plausible but remains unproven and should not be used to quantify individual leukaemia risk or modify radiotherapy schedules. The immediate value lies in defining testable hypotheses for occupational radiation research and chronobiology studies.