system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Antigens, CD34, Cell Lineage, Disease Progression, Disease-Free Survival, Female, Humans, Inflammation, Interleukin-17, Male, Middle Aged, Neovascularization, Pathologic, Neutrophils, Stomach Neoplasms, Tumor Microenvironment, Vascular Endothelial Growth Factor A.
user
Do interleukin-17-producing neutrophils link inflammatory stimuli to disease progression by promoting angiogenesis in gastric cancer? Context: Elevated levels of neutrophils have been associated with poor survival in various cancers, but direct evidence supporting a role for neutrophils in the immunopathogenesis of human cancers is lacking. A total of 573 gastric cancer (GC) patients were enrolled in this study. Immunohistochemistry and real-time PCR were performed to analyze the distribution and clinical relevance of neutrophils in different microanatomical regions. The regulation and function of neutrophils were assessed both in vitro and in vivo. Increased neutrophil counts in the peripheral blood were associated with poor prognosis in GC patients. In GC tissues, neutrophils were enriched predominantly in the invasive margin (IM), and neutrophil levels were a powerful predictor of poor survival in GC patients. Interleukin-17+ (IL-17) neutrophils constitute a large portion of IL-17-producing cells in human GC. Pro-inflammatory IL-17 is a critical mediator of the recruitment of neutrophils into the IM by CXC chemokines. Moreover, neutrophils at the IM were a major source of matrix metalloproteinase-9, a secreted protein that stimulates proangiogenic activity in GC cells. Accordingly, high levels of infiltrated neutrophils at the IM were positively correlated with angiogenesis progression of GC patients.
assistant
These data provide direct evidence supporting the pivotal role of neutrophils in GC progression and reveal a novel immune escape mechanism involving fine-tuned collaborative action between cancer cells and immune cells in the distinct tumor microenvironment. Final Decision: yes