胃癌腹膜转移是腹腔游离癌细胞与腹膜乳斑微环境双向作用的结果，通过前期研究我们发现由FAP+型肿瘤相关成纤维细胞、M2型肿瘤相关巨噬细胞以及乳斑缺氧微环境共同构筑的促转移微环境是胃癌腹膜转移的核心病理改变。由此我们提出：若阻断胃癌腹膜转移的病理进程，首先应该打破腹膜促转移微环境与胃癌细胞之间的动态平衡，消除腹膜促转移微环境对胃癌细胞的保护及支持机制，既可降低胃癌细胞的恶性程度及转移潜能，亦可增强胃癌细胞对辅助治疗的敏感性。本研究以优化腹膜微环境基质细胞靶向替换途径为核心研究内容，旨在通过肿瘤相关巨噬细胞、肿瘤相关成纤维细胞的外源性基因改造阻断胃癌腹膜转移病理进程。研究结果将为有效防治胃癌腹膜转移提供新的思路与靶点。

Gastric cancer peritoneal dissemination is the result of cross-talking between peritoneal free cancer cells and peritoneal milky spots microenvironment. Our previous studies revealed that the key pathological change of gastric cancer peritoneal dissemination is pro-metastatic soil which is composed by FAP+ tumor associated fibroblast, M2 phenotype tumor associated macrophage as well as peritoneal milky spots hypoxic microenvironment. Therefore we proposed that: the vital step to block gastric cancer peritoneal dissemination is breaking the dynamic balance between peritoneal free cancer cells and peritoneal milky spots microenvironment, eliminating the protection and supporting effect on peritoneal free cancer cells which is caused by peritoneal milky spots pro-metastasis microenvironment. By these means, the malignancy and metastatic potential of gastric cancer cells was restrained, and the sensitivity of gastric cancer cells to supportive chemical therapy may significantly enhanced. In this study, optimize the target-replacement pathway of stroma cells in peritoneal milky spots microenvironment is the key research content. We aim to block gastric cancer peritoneal dissemination by exogenous genetic remolding the tumor associated fibroblast and tumor associated macrophage. The results of present study will be valuable for further investigations of effective prevention and treatment of gastric cancer peritoneal dissemination.