Abstract
Obstructive sleep apnoea (OSA) is a prevalent disorder associated with increased cardiovascular, metabolic and neurocognitive morbidity. Recently, an increasing number of basic, clinical and epidemiological reports have suggested that OSA may also increase the risk of cancer, and adversely impact cancer progression and outcomes. This hypothesis is convincingly supported by biological evidence linking certain solid tumours and hypoxia, as well as by experimental studies involving cell and animal models testing the effects of intermittent hypoxia and sleep fragmentation that characterize OSA. However, the clinical and epidemiological studies do not conclusively confirm that OSA adversely affects cancer, even if they hold true for specific cancers such as melanoma. It is likely that the inconclusive studies reflect that they were not specifically designed to test the hypothesis or because of the heterogeneity of the relationship of OSA with different cancer types or even sub-types. This review critically focusses on the extant basic, clinical, and epidemiological evidence while formulating proposed directions on how the field may move forward.
Highlights
In recent years, a theoretical assumption has been formulated and posited that obstructive sleep apnoea (OSA) may adversely affect the incidence and outcomes of cancer [1,2,3]
Aggressiveness: apnoea–hypopnoea index (AHI) or DI4% values were associated with some markers of melanoma aggressiveness
Patients with a diagnosis of Obstructive sleep apnoea (OSA) had 1.14 (95%CI 1.10–1.18; p < 0·0001) increased probability to be subsequently diagnosed with melanoma compared to the non-OSA group at the end of the study
Summary
A theoretical assumption has been formulated and posited that obstructive sleep apnoea (OSA) may adversely affect the incidence and outcomes of cancer [1,2,3]. The biological framework for such putative associations is rather attractive, in light of the extensive previous fundamental work linking hypoxia and cancer [4,5]. The body of evidence that has accumulated to date has begun to unravel an understanding of several important pathophysiological mechanisms linking OSA and solid tumour biology. Some of the epidemiological data have enabled the realization that specific attributes of the tumour type as well as additional patient-related factors are critical operators, and determine whether an association between OSA and cancer incidence or outcomes will be either present or undetectable. We will critically review the basic, clinical, and epidemiological studies on this topic, and formulate some proposals on how the field could move forward
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