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Commentary |

Putative Links Between Sleep Apnea and CancerOSA and Cancer: From Hypotheses to Evolving Evidence

David Gozal, MD, FCCP; Ramon Farré, PhD; F. Javier Nieto, PhD
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From the Department of Pediatrics (Dr Gozal), Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Chicago, IL; the Unitat de Biofísica i Bioenginyeria (Dr Farré), Facultat de Medicina, Universitat de Barcelona-IDIBAPS, Barcelona, Spain; CIBER de Enfermedades Respiratorias (Dr Farré), Bunyola, Spain; and the Department of Population Health Sciences (Dr Nieto), School of Medicine and Public Health, University of Wisconsin, Madison, WI.

CORRESPONDENCE TO: David Gozal, MD, FCCP, Department of Pediatrics, Pritzker School of Medicine, The University of Chicago, 5721 S Maryland Ave, MC8000, K160, Chicago, IL 60637-1470; e-mail: dgozal@uchicago.edu


FUNDING/SUPPORT: Dr Gozal is supported by National Institutes of Health [Grant HL-65270] and the Herbert T. Abelson Endowed Chair in Pediatrics. Dr Farré is supported by Ministerio Español de Economia y Competitividad [Grant FIS-2014/00004] and SEPAR [2014-086]. Dr Nieto is supported in part by National Institutes of Health [Grant R01HL062252-11] and by the University of Wisconsin Helfaer Endowed Chair of Public Health.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(5):1140-1147. doi:10.1378/chest.15-0634
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In recent years, the potentially adverse role of sleep-disordered breathing in cancer incidence and outcomes has emerged. In parallel, animal models of intermittent hypoxia (IH) and sleep fragmentation (SF) emulating the two major components of OSA have lent support to the notion that OSA may enhance the proliferative and invasive properties of solid tumors. Based on several lines of evidence, we propose that OSA-induced increases in sympathetic outflow and alterations in immune function are critically involved in modifying oncologic processes including angiogenesis. In this context, we suggest that OSA, via IH (and potentially SF), promotes changes in several signaling pathways and transcription factors that coordinate malignant transformation and expansion, disrupts host immunologic surveillance, and consequently leads to increased probability of oncogenesis, accelerated tumor proliferation, and invasion, ultimately resulting in adverse outcomes.

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