Regulating surgical oncotaxis to improve the outcomes in cancer patients
Toshihiro Hirai1, Hideo Matsumoto, Hisako Kubota
1Department of Digestive Surgery, Kawasaki Medical School, 577 Matsushima, Kurashiki, 701-0192, Japan, hiro0928@med.kawasaki-m.ac.jp.
Abstract:
Excessive surgical stress and postoperative complications cause a storm of perioperative cytokine release, which has been shown to enhance tumor metastasis in experimental models. We have named this phenomenon "surgical oncotaxis". The mechanisms that underpin this process are thought to be excessive corticosteroid secretion, coagulopathy in the peripheral vasculature, immune suppression and excessive production of reactive oxygen species. Nuclear factor-kappa B (NFkB) activation plays a key role in these mechanisms. Minimally invasive surgical techniques should be used, and postoperative complications should be avoided whenever possible to lessen the impact of surgical oncotaxis. Furthermore, there may be a role for a small preoperative dose of corticosteroid or the use of free radical scavengers in the perioperative period. Recently, there has been a great deal of interest in omega-3 fatty acid, because it regulates NFkB activation. The use of multimodal treatments that regulate surgical oncotaxis may be as important as chemotherapy for determining the outcome of patients with cancer undergoing surgery.
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