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- W2500867121 abstract "Despite the undeniable medical advances achieved in recent decades, cancer remains one of the main causes of mortality. It is thus extremely important to make every effort to discover new risk factors for this disease, particularly ones that can be treated or modified. Various pathophysiologic pathways have been postulated as possible causes of cancer or its increased aggressiveness, and also of greater resistance to antitumoral treatment, in the presence of both intermittent hypoxia and sleep fragmentation (both inherent to sleep apnea). Thus far, these biological hypotheses have been supported by various experimental studies in animals. Meanwhile, recent human studies drawing on preexisting databases have observed an increase in cancer incidence and mortality in patients with a greater severity of sleep-disordered breathing. However, the methodologic limitations of these studies (which are mostly retrospective and lack any measurement of direct markers of intermittent hypoxia or sleep fragmentation) highlight the need for controlled, prospective studies that would provide stronger scientific evidence regarding the existence of this association and its main characteristics, as well as explore its nature and origin in greater depth. The great epidemiologic impact of both cancer and sleep apnea and the potential for clinical treatment make this field of research an exciting challenge. Despite the undeniable medical advances achieved in recent decades, cancer remains one of the main causes of mortality. It is thus extremely important to make every effort to discover new risk factors for this disease, particularly ones that can be treated or modified. Various pathophysiologic pathways have been postulated as possible causes of cancer or its increased aggressiveness, and also of greater resistance to antitumoral treatment, in the presence of both intermittent hypoxia and sleep fragmentation (both inherent to sleep apnea). Thus far, these biological hypotheses have been supported by various experimental studies in animals. Meanwhile, recent human studies drawing on preexisting databases have observed an increase in cancer incidence and mortality in patients with a greater severity of sleep-disordered breathing. However, the methodologic limitations of these studies (which are mostly retrospective and lack any measurement of direct markers of intermittent hypoxia or sleep fragmentation) highlight the need for controlled, prospective studies that would provide stronger scientific evidence regarding the existence of this association and its main characteristics, as well as explore its nature and origin in greater depth. The great epidemiologic impact of both cancer and sleep apnea and the potential for clinical treatment make this field of research an exciting challenge. ResponseCHESTVol. 150Issue 6PreviewAt the outset, we wish to thank Dr Marvisi1 for his interest in our article. As the authors of the letter have stated, in the past few years some outstanding research groups have described other pathophysiological pathways linking OSA with cancer, some orchestrated by hypoxia2-5 and some by sleep fragmentation.2-4,6,7 Some of these pathways are related to alterations to the immune system in macrophages/monocytes, natural killer cells, lymphocytes, and other immune cells.2-7 Interesting studies and reviews of the role of microvesicles/exosomes and the impact on the sympathetic/catecholaminergic system and other pathophysiological pathways have recently been published. Full-Text PDF Cancer and OSA: Beyond HypoxiaCHESTVol. 150Issue 6PreviewI have read with great interest and pleasure the excellent review by Martínez-García et al1 entitled “Cancer and OSA: Current Evidence from Human Studies” published in CHEST (August 2016). The authors shed light on this important and aporetical topic. Full-Text PDF" @default.
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- W2500867121 title "Cancer and OSA" @default.
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- W2500867121 doi "https://doi.org/10.1016/j.chest.2016.04.029" @default.
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