Abstract

Increased inspiratory oxygen concentration is constantly used during the perioperative period of cancer patients to prevent the potential development of hypoxemia and to provide an adequate oxygen transport to the organs, tissues and cells. Although the primary tumours are surgically removed, the effects of perioperative hyperoxia exposure on distal micro-metastases and on circulating cancer cells can potentially play a role in cancer progression or recurrence. In clinical trials, hyperoxia seems to increase the rate of postoperative complications and, by delaying postoperative recovery, it can alter the return to intended oncological treatment. The effects of supplemental oxygen on the long-term mortality of surgical cancer patients offer, at this point, conflicting results. In experimental studies, hyperoxia effects on cancer biology were explored following multiple pathways. In cancer cell cultures and animal models, hyperoxia increases the production of reactive oxygen species (ROS) and increases the oxidative stress. These can be followed by the induction of the expression of Brain-derived neurotrophic factor (BDNF) and other molecules involved in angiogenesis and by the promotion of various degrees of epithelial mesenchymal transition (EMT).

Highlights

  • The incidence of the main types of solid tumours is continuously rising around the world, despite increasing public awareness on modifiable risk factors and the implementation of preventive strategies, but this is related to advances in screening programs and diagnostic tools

  • The main cause of death is cancer progression, the occurrence of distal metastasis or cancer recurrence, as the vast majority of patients are successfully treated for primary tumours, with 64% of them having more than 5 years survival [3]

  • We further explored the relationship between hyperoxia and reactive oxygen species (ROS) production, the consecutive ROS signalling molecular pathways and the connection with angiogenesis and epithelial mesenchymal transition (EMT) as key biological processes that may foster and sustain cancer growth

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Summary

Background

The incidence of the main types of solid tumours is continuously rising around the world, despite increasing public awareness on modifiable risk factors and the implementation of preventive strategies, but this is related to advances in screening programs and diagnostic tools. For a long time considered as a useful and harmless intervention, oxygen therapy has been under scrutiny in recent years due to the accumulation of data regarding its deleterious effects in critically ill patients [14] and many areas of acute medicine (stroke, acute myocardial infarction, cardiac arrest) [15,16,17,18,19]. The optimal dose and duration for oxygen therapy in surgical cancer patients is not clearly established The purpose of this narrative review is to summarize and to critically review the currently available clinical and experimental evidence regarding the potential effects of hyperoxia exposure on cancer progression. We further explored the relationship between hyperoxia and reactive oxygen species (ROS) production, the consecutive ROS signalling molecular pathways and the connection with angiogenesis and epithelial mesenchymal transition (EMT) as key biological processes that may foster and sustain cancer growth

Hyperoxia Effects on Surgical Cancer Patients—Clinical and Experimental Data
Short-Term Effects of Hyperoxia in Surgical Patients
Respiratory Effects
Cardiovascular Effects
Cerebral Effects
Long-Term Effects of Hyperoxia on Surgical Cancer Patients
Results
ROS Production and Oxidative Stress
Hyperoxia and the Immune System
Design
Hyperoxic-Hypoxic Paradox
Conclusions
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