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Surgical excision is the cornerstone of treatment for solid tumors. Metastatic disease is the most important cause of cancer-related death patients affected with cancer. The likelihood of tumor metastases depends on the balance between the metastatic potential of the primary tumor and the antimetastatic host defenses. Among them, cell-mediated immunity and natural killer (NK) cell function are critical components.

A wealth of basic science data supports the hypothesis that the surgical stress response increases the likelihood of cancer dissemination during and after cancer surgery. Therefore, anesthetic management can potentially influence mid- and long-term outcome. Au contraire, surgery can inhibit major host defenses and promote the occurrence of metastases. Anesthetic techniques and drug choice also can affect the immune system. Together, these two interventions can have profound interactions with a patient’s immune defenses. The aims of this chapter are to review how the immune system can be influenced by surgery and anesthesia and discuss the possible mechanisms behind a potential benefit of one intervention over the other in this setting.


Intact immune responses to cancer cells are crucial in preventing and inhibiting tumor occurrence. The modern concept of immunoediting includes these processes: elimination, equilibrium, and escape.1,2 This implies that impairment in immune surveillance during the elimination process allows the escape of cancer cells from the protective immune attack. The appearance of clinically apparent tumors through the equilibrium process may occur, rendering the tumor cells more resistant to the immune system.

The NhK, CD4+ Th1 (T helper 1), and CD8+ CTL (cytotoxic lymphocyte) cells are the major antitumor immune effector cells, whereas Th2 (T helper 2), tumor-associated macrophages (TAM), and regulatory T (Treg) cells are the among the most important cells in the promotion of tumor settlement, growth, and progress by inhibiting the immune responses against cancer.3,4 Other mediators like proinflammatory cytokines,5 catecholamines,6 prostaglandins,6 and high levels of signal transducer and activator of transcription 3 (STAT3) factor activity7 are also involved in the process of postoperative metastases. NK cells have a crucial role particularly in eliminating metastases without prior sensitization and major histocompatibility complex (MHC) restriction.8 Therefore, preservation or activation of the function of NK cells is important. In this context, Th1 cells, characterized by interleukin (IL) 2, IL-12, and interferon gamma (IFN-γ) secretions are mandatory to induce antitumor CTL9 and to activate NK cells.8 On the other hand, Th2 cells differentiated by IL-4 and IL-10 can induce Th17 cells, Treg cells, TAMs, and myeloid derived suppressor cells (MDSCs),10 which have a major role in promoting tumor growth and metastasis by inhibiting antitumor immune responses like Th1 induction, CTL function, and NK activity.11

The role of proinflammatory cytokines (IL-6, tumor necrosis factor alpha [TNF-α], IL-13) should be outlined because release from ...

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