Obesity, sleep apnea, and cancer.

Autores de IIS La Fe

• 

  Miguel Ángel Martínez García

  Autor

Participantes ajenos a IIS La Fe

• Almendros I
• Farré R
• Gozal D

Grupos

• Neumología

  

  Leader

  Miguel Ángel Martínez García

Abstract

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.

Keywords

• WHITE ADIPOSE-TISSUE; TUMOR-ASSOCIATED MACROPHAGES; INTERMITTENT HYPOXIA; MOUSE MODEL; EXTRACELLULAR-MATRIX; INSULIN-RESISTANCE; CELL INVASION; BREAST-CANCER; INFLAMMATION; RISK