{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T06:05:24Z","timestamp":1781071524652,"version":"3.54.1"},"reference-count":52,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:00:00Z","timestamp":1781049600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100018036","name":"Nippon Shinyaku","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018036","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is an adult-onset autoinflammatory disorder driven by clonal hematopoiesis with somatic\n                      <jats:italic>UBA1<\/jats:italic>\n                      mutations. Azacitidine can reduce the mutant clonal burden and improve inflammatory manifestations. However, the clonal basis of treatment resistance remains poorly understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case presentation<\/jats:title>\n                    <jats:p>\n                      A 61-year-old man presented with predominant gastrointestinal symptoms, macrocytic anemia, thrombocytopenia, and systemic inflammation. A bone marrow examination revealed cytoplasmic vacuoles in myeloid precursors and trisomy 8. Retrospective genetic testing identified a somatic\n                      <jats:italic>UBA1<\/jats:italic>\n                      p.Met41Val variant, thus establishing the diagnosis of VEXAS syndrome in this patient. At the time of referral and during immunosuppressive therapy with prednisolone and cyclosporine, the\n                      <jats:italic>UBA1<\/jats:italic>\n                      variant allele frequency was consistently higher than the trisomy 8 burden, although relapse coincided with an expansion of trisomy 8. Azacitidine reduced the clonal burdens of both the\n                      <jats:italic>UBA1<\/jats:italic>\n                      mutation and trisomy 8. However, both persisted at similar levels, and after 21 cycles, the disease progressed to myelodysplastic syndrome with increased blasts-2, accompanied by concordant re-expansion of\n                      <jats:italic>UBA1<\/jats:italic>\n                      -mutated and trisomy 8 clones. These findings suggest that a trisomy 8 subclone likely emerged within a\n                      <jats:italic>UBA1<\/jats:italic>\n                      -mutated founder clone and expanded during treatment, whereas the disomy 8 fraction of the\n                      <jats:italic>UBA1<\/jats:italic>\n                      -mutated clone was preferentially eliminated by azacitidine. Urgent cord blood transplantation resulted in sustained clinical and molecular remission.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This case suggests that trisomy 8 may contribute to disease progression and azacitidine resistance in VEXAS syndrome.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1841156","type":"journal-article","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T05:40:09Z","timestamp":1781070009000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Trisomy 8 clonal expansion during disease progression and azacitidine resistance in VEXAS syndrome: a case report"],"prefix":"10.3389","volume":"17","author":[{"given":"Keijiro","family":"Sato","sequence":"first","affiliation":[{"name":"Department of Hematology, Japanese Red Cross 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