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Defining tumor-intrinsic determinants and microenvironmental, extrinsic factors that shape sensitivity or resistance to imipridones will identify actionable therapeutic opportunities and inform improved clinical strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To identify mechanisms of imipridone resistance, we obtained postmortem brain tissue from DMG patients who had received imipridones and\/or standard care. Single-nucleus RNA and open-chromatin sequencing were performed on N\u2009=\u200922 cases. Immunofluorescence-based myeloid phenotyping was performed on N\u2009=\u200946 cases. Mitochondrial copy-number analysis was performed on N\u2009=\u200919 cases. Validation of imipridone sensitivity, its effect on mitochondrial density, and its synergy with inhibition of mitochondrial biogenesis were assessed in DMG primary cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We established a single-cell RNA\/open-chromatin atlas from postmortem DMG cases and found imipridone treatment resulting in regressed mesenchymal transition, reduced myeloid-derived suppressive cells, and reversed aberrant H3K27-altered enhancer activity. Resistant tumors showed increased mitochondrial density, turnover, and membrane potential. Mitochondrial biogenesis and PPARGC1A emerged as resistance biomarkers and actionable targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These studies implicate mitochondrial biogenesis as a biomarker of imipridone resistance and a focus for the development of combinatorial strategies to provide effective therapeutic options for a challenging pediatric brain tumor.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag119","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T11:52:25Z","timestamp":1779450745000},"page":"2248-2262","source":"Crossref","is-referenced-by-count":3,"title":["Single-nucleus profiling of postmortem diffuse midline gliomas identifies mitochondrial biogenesis as a resistance mechanism to imipridone 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Jiangsu,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-2081-4173","authenticated-orcid":false,"given":"Weiqiang","family":"Yu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Common Mechanism Research for Major Diseases, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College , Suzhou, Jiangsu,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Laternser","sequence":"additional","affiliation":[{"name":"Children\u2019s Research Center, University Children\u2019s Hospital Zurich, University of Zurich , Zurich,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9539-7052","authenticated-orcid":false,"given":"Nalin","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, University of 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