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• W2740802932 abstract "Surgery is known to accelerate the growth and progression of metastases in patients undergoing oncological resections with 50-60% patients having recurrent metastasis after resection making it a major reason for treatment failure. This impedes the efficacy of adjuvant chemotherapy and overall prognosis of the patient. Studies have proved that inflammatory cascade initiated by surgery that increases metastatic growth and progression is mediated through a specific mechanism of neutrophil cell death called Neutrophil Extracellular Traps (NETs). We investigated the mechanism of how NET formation after surgical stress increases metastatic growth by influencing a pro-tumor microenvironment in order to specifically identify targets for perioperative therapy to keep metastases dormant and improve the effect of chemotherapy and overall prognosis. 12 week old male C57BL/6J mice (WT) and mice in which NET formation was inhibited, ie, WT mice injected with DNAse and global homozygous knockout of peptidyl arginine deaminase 4 (PAD4), an essential nuclear protein for NET formation, underwent splenic injection of 100,000 cells of the murine colorectal cancer cell line, MC-38, followed with either 70% hepatic ischemia-reperfusion (IR) for 60 minutes after 7 days or no IR. Livers were harvested at multiple time points and assessed for changes in both innate and adaptive immune cell populations by flow cytometry. On gross examination, the livers of the NET deficient mice had fewer tumors as compared to the WT mice. Mice, which underwent IR after tumor cell injection in both groups showed an increase in nodules formation versus those with just tumor cell injection, however were still more in WT than NET deficient mice. Flow cytometry revealed a decrease in both T H 17 (0.36% of T cells in no IR mice vs 0.0036% in IR mice) and CD8 cells (71% of T cells in no IR mice vs 34.8% in IR mice) in mice subjected to IR versus those with only tumor injection. We found that increased tumors after surgical stress, which were mediated by NET formation, were caused due to a decrease in anti-tumor activity of CD8 cells regulated via T H 17 cells. If controlled in the perioperative period, it may reduce acceleration in metastatic foci and improve the overall prognosis. We are further investigating the mechanism of NETs influencing the tumor immune environment. Citation Format: Vikas Sud, Samer Tohme, Dirk J. van der Windt, Hai Huang, Allan Tsung. T H 17: mediators of metastatic growth acceleration after surgery [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2940. doi:10.1158/1538-7445.AM2017-2940" @default.
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• W2740802932 date "2017-07-01" @default.
• W2740802932 modified "2023-09-26" @default.
• W2740802932 title "Abstract 2940: TH17: mediators of metastatic growth acceleration after surgery" @default.
• W2740802932 doi "https://doi.org/10.1158/1538-7445.am2017-2940" @default.
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