{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T19:20:45Z","timestamp":1788895245346,"version":"build-2803163510"},"reference-count":53,"publisher":"BMJ","issue":"6","license":[{"start":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T00:00:00Z","timestamp":1780444800000},"content-version":"unspecified","delay-in-days":2,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100001368","name":"V Foundation for Cancer Research","doi-asserted-by":"publisher","award":["V2024-026"],"award-info":[{"award-number":["V2024-026"]}],"id":[{"id":"10.13039\/100001368","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000646","name":"Japan Society for the Promotion of Science London","doi-asserted-by":"publisher","award":["25K20087"],"award-info":[{"award-number":["25K20087"]}],"id":[{"id":"10.13039\/501100000646","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["1R21CA297425-01A1"],"award-info":[{"award-number":["1R21CA297425-01A1"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001558","name":"Concern Foundation","doi-asserted-by":"publisher","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}],"id":[{"id":"10.13039\/100001558","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,5,14]]},"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>High-grade serous carcinoma (HGSC) of the ovary acquires chemoresistance through diverse cancer cell-intrinsic and cell-extrinsic mechanisms, culminating in treatment-refractory intraperitoneal metastasis. Previous work suggests that chemotherapy induces immunological changes in the tumor microenvironment (TME). However, experimental evidence for how such chemotherapy-induced TME remodeling modulates the response to ongoing chemotherapy remains poorly documented in HGSC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed paired pre-chemotherapy and post-chemotherapy HGSC bulk transcriptomic and single-cell RNA sequencing (scRNA-seq) datasets to identify chemotherapy-induced tumor-extrinsic factors and their cellular sources in the TME. To test causality, we used chemoresistant, homologous recombination-proficient murine metastatic HGSC models with deficiencies in the interleukin 1 beta (IL1\u03b2) pathway (IL1\u03b2\u2013interleukin 1 receptor type 1 (IL1R1) axis). Flow cytometry and scRNA-seq of omental tumors were used to define cellular interactions. Contributions of neutrophils and neutrophil extracellular traps (NETs) were assessed by antibody-mediated depletion and immunofluorescence. Direct effects of IL1\u03b2 and NETs on cancer cell chemosensitivity were tested in vitro. Finally, paired pre-chemotherapy and post-chemotherapy omental HGSC specimens from patients were analyzed for neutrophil infiltration and NET formation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In HGSC datasets, post-chemotherapy tumors exhibited increased IL1\u03b2 expression with myeloid cells identified as the primary source. In chemoresistant murine models, chemotherapy increased neutrophils and NETs in omentum tumors in wild-type mice. These increases were abrogated in IL1\u03b2-deficient mice, which showed a shift toward an effector-like CD8\n                      <jats:sup>+<\/jats:sup>\n                      T-cell state and improved tumor control. Neutrophil depletion in wild-type mice recapitulated the chemosensitive phenotype of IL1\u03b2-deficient mice. In vitro, IL1\u03b2 did not alter cancer cell-intrinsic chemosensitivity, whereas NETs reduced the chemosensitivity of cancer cells. Furthermore, scRNA-seq and flow cytometry revealed that IL1R1 was predominantly expressed by tumor-associated fibroblasts. Consistently, IL1R1-deficient mice exhibited increased chemosensitivity, with decreased neutrophil accumulation and increased IFN\u03b3\n                      <jats:sup>+<\/jats:sup>\n                      TNF\n                      <jats:sup>+<\/jats:sup>\n                      CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells. Additionally, we found that chemotherapy upregulated the neutrophil chemoattractant C-X-C motif chemokine ligand 2 (CXCL2), and disruption of the IL1\u03b2\u2013IL1R1 axis decreased CXCL2 levels in tumor-associated fibroblasts. Finally, residual human HGSC tumors after chemotherapy showed increased neutrophils and a trend toward increased NETs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We demonstrate that chemotherapy-induced IL1\u03b2-dependent neutrophil accumulation drives chemoresistance in HGSC. This study provides experimental evidence that chemotherapy-induced inflammation contributes to chemoresistance and highlights the potential of targeting this pathway to overcome chemoresistance in HGSC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-014253","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T16:15:11Z","timestamp":1780503311000},"page":"e014253","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Chemotherapy induces an IL1\u03b2-dependent neutrophil recruitment and activation that promote chemoresistance in metastatic ovarian cancer"],"prefix":"10.1136","volume":"14","author":[{"given":"Taito","family":"Miyamoto","sequence":"first","affiliation":[{"name":"Wistar Institute, Philadelphia, Pennsylvania, USA"},{"name":"Gynecology and Obstetrics, Graduate School of Medicine, Kyoto University, Kyoto, 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