Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Molecular Mechanisms of Cancer-Induced Sleep Disruption

Version 1 : Received: 1 May 2019 / Approved: 6 May 2019 / Online: 6 May 2019 (08:52:31 CEST)

A peer-reviewed article of this Preprint also exists.

Walker, W.H., II; Borniger, J.C. Molecular Mechanisms of Cancer-Induced Sleep Disruption. Int. J. Mol. Sci. 2019, 20, 2780. Walker, W.H., II; Borniger, J.C. Molecular Mechanisms of Cancer-Induced Sleep Disruption. Int. J. Mol. Sci. 2019, 20, 2780.

Abstract

Sleep is essential for health. Indeed, poor sleep is consistently linked to the development of systemic disease, including depression, metabolic syndrome, and cognitive impairments. Further evidence has accumulated suggesting a role for sleep in cancer initiation and progression (primarily breast cancer). Indeed, patients with cancer and cancer survivors frequently experience poor sleep, manifested as insomnia, circadian misalignment, hypersomnia, somnolence syndrome, hot flushes, and nightmares. These problems are associated with a reduction in patients’ quality of life and increased mortality. Due to the heterogeneity among cancers, treatment regimens, patient populations, and lifestyle factors, the etiology of cancer-induced sleep disruption is largely unknown. Here, we discuss recent advances in understanding the pathways linking cancer and the brain and how this leads to altered sleep patterns. We describe a conceptual framework where tumors disrupt normal homeostatic processes, resulting in aberrant changes in physiology and behavior that are detrimental to health. Finally, we discuss how this knowledge can be leveraged to develop novel therapeutic approaches for cancer-associated sleep disruption, with special emphasis on host-tumor interactions.

Keywords

breast cancer; sleep; IL-6; hypocretin/orexin; leptin; EEG; autonomic nervous system

Subject

Biology and Life Sciences, Cell and Developmental Biology

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