Surgery-mediated tumor-promoting effects on the immune microenvironment

Area of Science:

• Oncology
• Immunology
• Surgical Science

Background:

• Surgical resection remains a primary cancer treatment, but it can paradoxically promote metastasis.
• Surgery triggers inflammation, leading to the formation of a tumor microenvironment (TME) that supports cancer growth and spread.

Purpose of the Study:

• To review the pro-tumorigenic mechanisms initiated by surgery.
• To explore how surgery impacts cellular components within the tumor microenvironment.
• To identify potential targets for perioperative therapeutic strategies.

Main Methods:

• Literature review of studies on surgery, cancer metastasis, and the tumor microenvironment.
• Analysis of cellular and molecular responses to surgical insult.
• Synthesis of findings on platelet, neutrophil, macrophage, and immune cell involvement.

Main Results:

• Surgery induces circulating tumor cell (CTC) dissemination and activates platelets, neutrophils, and macrophages.
• These activated cells form structures like neutrophil extracellular traps (NETs) and create a supportive TME.
• Surgery also leads to immunosuppression by expanding regulatory T cells and myeloid-derived suppressor cells while suppressing natural killer (NK) cells.

Conclusions:

• Surgery-induced cellular changes and inflammation create a pro-metastatic environment.
• These mechanisms contribute to postoperative cancer recurrence and metastasis.
• Targeting these perioperative events may prevent surgery-associated cancer spread.