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However, the intricate dynamics within the peritoneal microenvironment (PME) during the treatment process remain largely unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Matched samples from primary tumours (PT), peritoneal metastases (PM), and paired pre\u2010treatment and post\u2010chemo\/immunotherapy (anti\u2010PD\u20101\/PD\u2010L1) progression malignant ascites samples, were collected from 48 patients. These samples were subjected to single\u2010cell RNA sequencing (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a030), multiplex immunofluorescence (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a030), and spatial transcriptomics (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a03). Furthermore, post hoc analyses of a phase 1 clinical trial (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a020, NCT03710265) and an in\u2010house immunotherapy cohort (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a0499) were conducted to validate the findings.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Tracing the evolutionary trajectory of epithelial cells unveiled the terminally differentially MUC1+ cancer cells with a high epithelial\u2010to\u2010mesenchymal transition potential, and they demonstrated spatial proximity with fibroblasts and endothelial cells, correlating with poor prognosis. A significant expansion of macrophage infiltrates, which exhibited the highest proangiogenic activity, was observed in the ascites compared with PT and PM. Besides, higher C1Q+ macrophage infiltrates correlated with significantly lower GZMA+ T\u2010lymphocyte infiltrates in therapeutic failure cases, potentially mediated by the LGALS9\u2010CD45 and SPP1\u2010CD44 ligand\u2013receptor interactions. In the chemoresistant group, intimate interactions between C1Q+ macrophages and fibroblasts through the complement activation pathway were found. In the group demonstrating immunoresistance, heightened TGF\u2010\u03b2 production activity was detected in MUC1+ cancer cells, and they were skewed to interplay with C1Q+ macrophages through the GDF15\u2010TGF\u2010\u03b2R2 axis. Ultimately, post hoc analyses indicated that co\u2010targeting TGF\u2010\u03b2 and PDL1 pathways may confer superior clinical benefits than sole anti\u2010PD\u20101\/PD\u2010L1 therapy for patients presenting with GCPM at the time of diagnosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings elucidated the cellular differentiation trajectories and crucial drug resistance features within PME, facilitating the exploration of effective targets for GCPM treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>MUC1+ cancer cells with a high epithelial\u2010to\u2010mesenchymal transition potential and exhibiting spatial proximity to fibroblasts and endothelial cells constitute the driving force of gastric cancer peritoneal metastasis (GCPM).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Higher C1Q+ macrophage infiltrates correlated with significantly lower GZMA+ T\u2010lymphocyte infiltrates within the peritoneal microenvironment in therapeutic failure cases.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Co\u2010targeting TGF\u2010\u03b2 and PDL1 pathways may confer superior clinical benefits than sole anti\u2010PD\u20101\/PD\u2010L1 therapy for patients presenting with GCPM at diagnosis.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  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