{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:34:22Z","timestamp":1791228862069,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T00:00:00Z","timestamp":1775088000000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Medicine"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study aimed to investigate the relationship between gut microbiota and chemotherapy\u2010induced nausea and vomiting (CINV) in patients with ovarian cancer undergoing platinum\u2010based chemotherapy (carboplatin or cisplatin combined with paclitaxel).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Clinical data and fecal samples were collected from patients with ovarian cancer after admission but prior to the initiation of their first chemotherapy cycle. Patients were divided into the CINV (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200925) and non\u2010CINV (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200925) groups on the basis of symptoms occurring after chemotherapy. No additional samples were collected during chemotherapy. Integrated metagenomic sequencing and untargeted metabolomic profiling identified CINV\u2010associated microbial taxa and metabolites. Additionally, fecal microbiota transplantation (FMT) in SD rats validated causal links between gut dysbiosis and CINV pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Bacteroides caccae<\/jats:italic>\n                      <\/jats:styled-content>\n                      , Corynebacteriales, and\n                      <jats:italic>Corynebacterium<\/jats:italic>\n                      were significantly enriched in the CINV group. KEGG enrichment revealed upregulated pathways in CINV, including focal adhesion, lysosome function, and eukaryotic cellular communities. Metabolomic analysis identified 19 significantly increased metabolites in the fecal samples of CINV patients versus 10 in non\u2010CINV controls. KEGG enrichment revealed that the pentose phosphate pathway, glutathione metabolism, and lipoic acid metabolism were significantly implicated in CINV pathogenesis. Multi\u2010omics integration revealed\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      sp. A1C1 strongly correlated with hesperetin, arbutin, orciprenaline, and myristolic acid. In rats, cisplatin\u2010induced CINV models showed higher kaolin consumption versus controls (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). FMT from non\u2010CINV donors reduced kaolin consumption in cisplatin\u2010treated rats (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). The expression of 5\u2010HT3R, NK1R, and NK2R in the medulla oblongata and colon was significantly increased in the cisplatin model group (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05) and partially reversed by non\u2010CINV FMT (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Gut microbiota dysbiosis directly contributes to CINV pathogenesis.\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      sp. A1C1 and its putatively identified metabolites (hesperetin, arbutin, orciprenaline, and myristolic acid) represent potential diagnostic biomarkers for CINV.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cam4.71752","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T10:57:00Z","timestamp":1775127420000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The Role of Gut Microbiota and Their Derived Metabolites in Chemotherapy\u2010Induced Nausea and Vomiting in Ovarian Cancer"],"prefix":"10.1002","volume":"15","author":[{"given":"Shuiling","family":"Zu","sequence":"first","affiliation":[{"name":"Department of Gynecology, Fujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics &amp; Gynecology and Pediatrics Fujian Medical University  Fuzhou China"},{"name":"School of Nursing Fujian Medical University  Fuzhou 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