• Miguel Ángel Martínez-García, Francisco Campos-Rodriguez, and Ferrán Barbé.
• Respiratory Department, Hospital Universitario y Politécnico La Fe, Valencia, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Madrid, Spain. Electronic address: mianmartinezgarcia@gmail.com.
• Chest. 2016 Aug 1; 150 (2): 451-63.

AbstractDespite 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.Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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