{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T07:02:37Z","timestamp":1784617357350,"version":"3.55.0"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T00:00:00Z","timestamp":1780963200000},"content-version":"vor","delay-in-days":159,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Else Kr\u00f6ner Fresenius Stiftung","award":["2019_Kolleg_14"],"award-info":[{"award-number":["2019_Kolleg_14"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Dexamethasone (DEXA) is the routine therapy for tumor- or treatment-associated edema management in glioblastoma, whereas bevacizumab (BEV) is increasingly used as a steroid-sparing alternative. Although both reduce edema, their broader immunometabolic effects remain ill-defined. Here, we examine how DEXA and BEV differentially affect tumor metabolism and microenvironment in patient samples and experimental models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated 1H-NMR-based metabolomics of human glioblastoma specimens with mechanistic in vitro studies to compare DEXA and BEV. Microenvironmental modulation by DEXA vs BEV was further investigated in vivo in a syngeneic, immunocompetent orthotopic glioma mouse model by flow cytometry and immunohistochemistry, followed by ex vivo co-culture models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Tumors from DEXA-treated patients (n\u2009=\u200912) vs steroid-naive controls (n\u2009=\u200918) showed nine significantly altered metabolites, including increased lactate, cystathionine, and 2-hydroxybutyrate, indicating a metabolically accelerated, proliferation-associated state. In an immunocompetent orthotopic glioma model, DEXA reduced intratumoral T cell infiltration and induced cytokine conditions favoring regulatory T cells (Tregs) and myeloid recruitment. In contrast, BEV elicited a coordinated immunostimulatory phenotype: it increased chemotactic cytokines in vitro (eg CCL5), decreased intratumoral Tregs (CD4+FOXP3+), enhanced activated, Granzyme B (GzmB) expressing effector T cells (CD4+GzmB+) in vivo, and improved spleenocyte-mediated tumor cell killing ex vivo.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Together, DEXA promotes an immunosuppressive, metabolically active tumor microenvironment, whereas BEV supports immune infiltration and activation. These data, combining tissue-derived metabolomics with functional and mechanistic studies in vitro, ex vivo, and in vivo, reveal fundamentally divergent immunometabolic effects of anti-edematous therapies with direct implications in clinical practice, particularly alongside immunotherapy in glioblastoma.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/noajnl\/vdag147","type":"journal-article","created":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T11:42:47Z","timestamp":1780659767000},"source":"Crossref","is-referenced-by-count":0,"title":["Differential modulation of glioma metabolism and the tumor microenvironment following dexamethasone and bevacizumab treatment"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-4918-9502","authenticated-orcid":false,"given":"Louise","family":"Maise","sequence":"first","affiliation":[{"name":"Department of Neurology & Interdisciplinary Neuro-Oncology, University Hospital Tuebingen, Hertie Institute 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