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10.1158/0008-5472.CAN-15-1591 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-1591 C4794393!4794393 !26759232     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26759232 &cmd=llinks): Failed to open stream: HTTP request failed! 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Neutrophil Extracellular Traps Promote the Development and Progression of Liver Metastases after Surgical Stress |pdf=|usr=}}{{26759232 }} gab.com Text Neutrophil Extracellular Traps Promote the Development and Progression of Liver Metastases after Surgical Stress JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26759232 #FOAvip Risks of tumor recurrence after surgical resection have been known for decades, but the mechanisms underlying treatment failures remain poorly understood. Neutrophils, first-line responders after surgical stress, may play an important role in linking inflammation to cancer progression. In response to stress, neutrophils can expel their protein-studded chromatin to form local snares known as neutrophil extracellular traps (NET). In this study, we asked whether, as a result of its ability to ensnare moving cells, NET formation might promote metastasis after surgical stress. Consistent with this hypothesis, in a cohort of patients undergoing attempted curative liver resection for metastatic colorectal cancer, we observed that increased postoperative NET formation was associated with a >4-fold reduction in disease-free survival. In like manner, in a murine model of surgical stress employing liver ischemia-reperfusion, we observed an increase in NET formation that correlated with an accelerated development and progression of metastatic disease. These effects were abrogated by inhibiting NET formation in mice through either local treatment with DNAse or inhibition of the enzyme peptidylarginine deaminase, which is essential for NET formation. In growing metastatic tumors, we found that intratumoral hypoxia accentuated NET formation. Mechanistic investigations in vitro indicated that mouse neutrophil-derived NET triggered HMGB1 release and activated TLR9-dependent pathways in cancer cells to promote their adhesion, proliferation, migration, and invasion. Taken together, our findings implicate NET in the development of liver metastases after surgical stress, suggesting that their elimination may reduce risks of tumor relapse. Twit Text FOAVip Neutrophil Extracellular Traps Promote the Development and Progression of Liver Metastases after Surgical Stress ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26759232 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26759232 #FOAvip English Wikipedia <ref>{{Cite pmid|26759232 }}</ref> Neutrophil Extracellular Traps Promote the Development and Progression of Liver Metastases after Surgical Stress #MMPMID26759232 Tohme S ; Yazdani HO ; Al-Khafaji AB ; Chidi AP ; Loughran P ; Mowen K ; Wang Y ; Simmons RL ; Huang H ; Tsung A Cancer Res 2016[Mar]; 76 (6 ): 1367-80 PMID26759232 show ga Risks of tumor recurrence after surgical resection have been known for decades, but the mechanisms underlying treatment failures remain poorly understood. Neutrophils, first-line responders after surgical stress, may play an important role in linking inflammation to cancer progression. In response to stress, neutrophils can expel their protein-studded chromatin to form local snares known as neutrophil extracellular traps (NET). In this study, we asked whether, as a result of its ability to ensnare moving cells, NET formation might promote metastasis after surgical stress. Consistent with this hypothesis, in a cohort of patients undergoing attempted curative liver resection for metastatic colorectal cancer, we observed that increased postoperative NET formation was associated with a >4-fold reduction in disease-free survival. In like manner, in a murine model of surgical stress employing liver ischemia-reperfusion, we observed an increase in NET formation that correlated with an accelerated development and progression of metastatic disease. These effects were abrogated by inhibiting NET formation in mice through either local treatment with DNAse or inhibition of the enzyme peptidylarginine deaminase, which is essential for NET formation. In growing metastatic tumors, we found that intratumoral hypoxia accentuated NET formation. Mechanistic investigations in vitro indicated that mouse neutrophil-derived NET triggered HMGB1 release and activated TLR9-dependent pathways in cancer cells to promote their adhesion, proliferation, migration, and invasion. Taken together, our findings implicate NET in the development of liver metastases after surgical stress, suggesting that their elimination may reduce risks of tumor relapse. |Animals [MESH] |Cell Adhesion/physiology [MESH] |Cell Movement/physiology [MESH] |Cell Proliferation/physiology [MESH] |Disease Progression [MESH] |Extracellular Traps/metabolism/*physiology [MESH] |HMGB1 Protein/metabolism [MESH] |Humans [MESH] |Liver/metabolism/*pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neoplasm Metastasis/*pathology [MESH] |Neoplasm Recurrence, Local/metabolism/pathology [MESH] |Neutrophils/metabolism/*pathology [MESH]Neutrophil Extracellular Traps Promote the Development and Progression(epmc).pdf DeepDyve Pubget Overpricing