Publication | Open Access
Shift work and cancer – considerations on rationale, mechanisms, and epidemiology
236
Citations
144
References
2010
Year
PathologyGynecologyCancer BiologyOncologyShift WorkCircadian DisruptionPublic HealthRadiation OncologyCancer ResearchSleepAlertnessMedicineEndocrinologySleep DeprivationMelatoninEndocrine-related CancerCancer EpidemiologyBreast CancerCircadian RhythmCancer GrowthChronobiology
The mechanisms by which circadian disruption may favor the induction and/or promotion of malignant tumors are complex and multifactorial. This paper summarizes the rationale for, possible mechanisms of, and problems related to risk assessment of the association between shift work and cancer. Circadian disruption induces multilevel endocrine changes, such as melatonin suppression by light at night that targets endocrine‑responsive breast and possibly prostate tissue, causes repeated phase shifting that disrupts circadian cell‑cycle regulation and promotes uncontrolled growth, and leads to sleep deprivation that suppresses immune surveillance and permits malignant clone establishment or growth. The epidemiological studies published so far, although dealing with large cohorts and controlling for several personal confounders, have defined the exposure to shift and/or night work rather loosely and consequently do not allow for the proper assessment of the risk connected with circadian disruption.
This paper summarizes the rationale for, possible mechanisms of, and problems related to risk assessment of the association between shift work and cancer. The mechanisms by which circadian disruption may favor the induction and/or promotion of malignant tumors are complex and multifactorial. The multilevel endocrine changes caused by circadian disruption with melatonin suppression through light at night (LAN) lead to the oncogenic targeting of the endocrine-responsive breast in women and possibly the prostate in men. Repeated phase shifting with internal desynchronization may lead to defects in the regulation of the circadian cell cycle, thus favoring uncontrolled growth. Sleep deprivation leads to the suppression of immune surveillance that may permit the establishment and/or growth of malignant clones. The epidemiological studies published so far, although dealing with large cohorts and controlling for several personal confounders, have defined the exposure to shift and/or night work rather loosely and consequently do not allow for the proper assessment of the risk connected with circadian disruption.
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