It is well-known that cancer surgery can actually promote the growth of some tumors by a variety of mechanisms. There are observational data suggesting that surgery per se can increase the risk of cancer among individuals without a history of clinical cancer. Occult microscopic cancers are exceedingly common in the general population and are held in a dormant state by a balance between cell proliferation and cell death and also an intact host immune surveillance. The catecholamine surge from the stress of surgery and resulting β(2)-adrenergic signaling culminates in a transient and robust increased vascular endothelial growth factor expression locally and systemically that is enough to start tumor angiogenesis and end dormancy. The same catecholamine surge and β(2)-adrenergic signaling impairs cell-mediated immunity at a crucial time. Elegant animal studies have demonstrated that perioperative nonselective β-blockade abrogates surgical stress-induced angiogenesis and tumor growth. Prospective human trials are desperately needed and clinical implications are discussed.
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Luca Mascitelli (2011) studied this question.
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