Sleep apnoea and cancer: the new challenge.

Obstructive sleep apnoea (OSA) is a well-known public health problem owing to its high prevalence and the numerous consequences of the disorder, including excessive daytime somnolence, cognitive impairment and consequently traffic accidents [1]. There is an excess in cardiovascular mortality that has been repeatedly reported in longitudinal cohorts, in both general and clinical populations. Despite many confounding factors, including age, sex and obesity, evidence has accumulated over the past 25 years regarding strong associations between OSA, cardiovascular diseases i.e. hypertension [2], coronary artery disease, cerebrovascular disease, heart rate and conduction disorders, and excess mortality. Through a complex interaction between obesity, metabolism, sleep and sleep apnoea, metabolism seems to be altered by OSA [3], although it remains uncertain whether treating OSA may improve blood glucose control, lipid metabolism [4] or adipose tissue distribution [5]. More recently, it has been suspected that the excess in mortality in OSA could not only be attributed to cardiometabolic consequences but also to cancer. Cancer has been found to be associated with sleep disordered breathing (SDB) in two large observational studies [6, 7]. This had been previously suspected through proof-of-concept animal studies that demonstrated an association between intermittent hypoxia, a major consequence of SDB, carcinogenesis and acceleration of tumour growth [8]. Intermittent hypoxia is a particular condition with relatively specific cellular effects [9], including changes in host immune responses that could favour cancer progression [10]. The relationship between SDB and cancer has been studied in animal [8, 11, 12] and clinical studies; they suggest that SDB, mainly through intermittent hypoxia, is likely to be associated with an increase in growth rate [8], incidence [6] and mortality [7] of cancer. In addition, sleep fragmentation, another hallmark of sleep apnoea, has also been demonstrated to promote tumour progression in animal models through recruitment of tumourassociated macrophages and Toll-like receptor 4 signalling pathways [13].