Surgical Stress Promotes Tumor Progression: A Focus on the Impact of the Immune Response.
Amblessed E OnumaHongji ZhangLindsay A GilHai HuangAllan TsungPublished in: Journal of clinical medicine (2020)
Despite advances in systemic therapies, surgery is crucial for the management of solid malignancy. There is increasing evidence suggesting that the body's response to surgical stress resulting from tumor resection has direct effects on tumor cells or can alter the tumor microenvironment. Surgery can lead to the activation of early and key components of the innate and adaptative immune systems. Platelet activation and the subsequent pro-coagulation state can accelerate the growth of micrometastases. Neutrophil extracellular traps (NETs), an extracellular network of DNA released by neutrophils in response to inflammation, promote the adhesion of circulating tumor cells and the growth of existing micrometastatic disease. In addition, the immune response following cancer surgery can modulate the tumor immune microenvironment by promoting an immunosuppressive state leading to impaired recruitment of natural killer (NK) cells and regulatory T cells (Tregs). In this review, we will summarize the current understanding of mechanisms of tumor progression secondary to surgical stress. Furthermore, we will describe emerging and novel peri-operative solutions to decrease pro-tumorigenic effects from surgery.
Keyphrases
- immune response
- minimally invasive
- coronary artery bypass
- regulatory t cells
- circulating tumor cells
- dendritic cells
- nk cells
- circulating tumor
- poor prognosis
- stem cells
- oxidative stress
- toll like receptor
- escherichia coli
- papillary thyroid
- coronary artery disease
- squamous cell carcinoma
- percutaneous coronary intervention
- single molecule
- squamous cell
- biofilm formation
- network analysis
- childhood cancer
- nucleic acid