The interest on a potential association between
cancer and
sleep-disordered breathing (SDB) has clearly gained substantial
traction over the last several years. This novel relationship was initially explored in experimental models of
obstructive sleep apnea (OSA) and showed that both intermittent
hypoxia and
sleep fragmentation, the two main hallmarks of OSA, promoted alterations in both
tumorigenesis and
tumor malignant properties. In parallel, an intriguing role of
obesity as a major interactive player in the relationship between
cancer and OSA was postulated in the following contextual settings: (1)
obesity (with or without OSA) is associated with increased risk of some types of
cancer (both incidence and aggressiveness), whereas
obesity could be protective for others ("obesity paradox"); (2) OSA has been associated with increased risk for some types of
cancer (independent of
obesity), but not with others; (3) More than 80% of adult patients with OSA are
overweight and >50% are obese; (4) both OSA and
obesity exhibit oscillations in tissue
oxygen tensions in peripheral organs such as adipose tissues. Further understanding these complex relationships become all the more important considering that the prevalence of
obesity,
cancer and OSA are all increasing worldwide. In parallel, experimental models of OSA provide biological plausibility constructs to the clinical and epidemiological findings, suggesting that the metabolic and inflammatory changes induced by chronic intermittent
hypoxia and
sleep fragmentation may foster or exacerbate immune and biomechanical alterations of the tumor microenvironment, including the expression of extracellular matrix components facilitating
tumor progression.