Almendros Isaac, Martinez-Garcia Miguel A, Farré Ramon, Gozal David
Unitat de Biofísica i Bioenginyeria, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Barcelona, Spain.
Centro de Investigación Biomédica en Red en Enfermedades Respiratorias (CIBERES), Madrid, Spain.
Int J Obes (Lond). 2020 Aug;44(8):1653-1667. doi: 10.1038/s41366-020-0549-z. Epub 2020 Feb 18.
The interest on a potential association between cancer and sleep-disordered breathing (SDB) has clearly gained substantial traction over the last several years. This novel relationship was initially explored in experimental models of obstructive sleep apnea (OSA) and showed that both intermittent hypoxia and sleep fragmentation, the two main hallmarks of OSA, promoted alterations in both tumorigenesis and tumor malignant properties. In parallel, an intriguing role of obesity as a major interactive player in the relationship between cancer and OSA was postulated in the following contextual settings: (1) obesity (with or without OSA) is associated with increased risk of some types of cancer (both incidence and aggressiveness), whereas obesity could be protective for others ("obesity paradox"); (2) OSA has been associated with increased risk for some types of cancer (independent of obesity), but not with others; (3) More than 80% of adult patients with OSA are overweight and >50% are obese; (4) both OSA and obesity exhibit oscillations in tissue oxygen tensions in peripheral organs such as adipose tissues. Further understanding these complex relationships become all the more important considering that the prevalence of obesity, cancer and OSA are all increasing worldwide. In parallel, experimental models of OSA provide biological plausibility constructs to the clinical and epidemiological findings, suggesting that the metabolic and inflammatory changes induced by chronic intermittent hypoxia and sleep fragmentation may foster or exacerbate immune and biomechanical alterations of the tumor microenvironment, including the expression of extracellular matrix components facilitating tumor progression.
在过去几年中，癌症与睡眠呼吸紊乱（SDB）之间潜在关联的研究明显获得了大量关注。这种新关系最初是在阻塞性睡眠呼吸暂停（OSA）的实验模型中进行探索的，结果表明，间歇性缺氧和睡眠片段化这两个OSA的主要特征，均促进了肿瘤发生和肿瘤恶性特性的改变。与此同时，在以下背景下推测了肥胖作为癌症与OSA关系中的主要交互因素所起的有趣作用：（1）肥胖（无论有无OSA）与某些类型癌症的风险增加相关（包括发病率和侵袭性），而肥胖对其他一些癌症可能具有保护作用（“肥胖悖论”）；（2）OSA与某些类型癌症的风险增加相关（独立于肥胖），但与其他癌症无关；（3）超过80%的成年OSA患者超重，超过50%的患者肥胖；（4）OSA和肥胖在外周器官如脂肪组织中的组织氧张力均表现出波动。鉴于肥胖、癌症和OSA在全球范围内的患病率都在上升，进一步了解这些复杂关系变得尤为重要。与此同时，OSA的实验模型为临床和流行病学研究结果提供了生物学合理性解释，表明慢性间歇性缺氧和睡眠片段化所诱导的代谢和炎症变化可能促进或加剧肿瘤微环境的免疫和生物力学改变，包括促进肿瘤进展的细胞外基质成分的表达。
