{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T13:50:49Z","timestamp":1781877049121,"version":"3.54.5"},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T00:00:00Z","timestamp":1775260800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T00:00:00Z","timestamp":1775260800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270144"],"award-info":[{"award-number":["82270144"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Pediatric myelodysplastic syndromes (MDS) differ from adult MDS, and their genetic basis is poorly understood. This study characterizes the genomic features and clinical outcomes of advanced pediatric MDS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this retrospective study, next\u2010generation sequencing was performed on 63 pediatric patients with advanced MDS, including 46 with MDS with excess blasts (MDS\u2010EB) and 17 with MDS\u2010EB in transformation (MDS\u2010EB\u2010T, 2016 WHO classification), to detect somatic and potential germline variants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Mutations in 53 genes were detected in 49 patients (77.8%), with a median of 2 variants per patient (range, 0\u20138). Alterations in the RAS\/MAPK pathway were most common, occurring in 28 patients (44.4%). Monosomy 7 significantly co\u2010occurred with\n                      <jats:italic>SETBP1<\/jats:italic>\n                      ,\n                      <jats:italic>ETV6<\/jats:italic>\n                      , and\n                      <jats:italic>GATA2<\/jats:italic>\n                      mutations (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01). Time\u2010dependent analyses showed HSCT improved 2\u2010year overall survival (OS, 42.6% vs. 84.5%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.003) and event\u2010free survival (EFS, 37.3% vs. 58.2%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.011). In multivariate analyses, HSCT was strongly associated with improved OS and EFS (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01).\n                      <jats:italic>PTPN11<\/jats:italic>\n                      mutation remained an independent predictor of poorer OS and EFS (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05), and MDS\u2010EB\u2010T subtype independently predicted inferior EFS (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      In advanced pediatric MDS, HSCT was associated with improved survival, whereas\n                      <jats:italic>PTPN11<\/jats:italic>\n                      mutations emerged as an adverse prognostic factor.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ejh.70182","type":"journal-article","created":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T10:44:33Z","timestamp":1775299473000},"page":"235-244","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genomic Landscape and Clinical Outcomes of Advanced Pediatric Myelodysplastic Syndromes"],"prefix":"10.1111","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-3252-4856","authenticated-orcid":false,"given":"Chenmeng","family":"Liu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology &amp; Blood Diseases Hospital Chinese Academy of Medical Sciences &amp; Peking Union Medical College  Tianjin China"},{"name":"Tianjin Institute of Health Science  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-2107-8536","authenticated-orcid":false,"given":"Xingchen","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology &amp; Blood Diseases Hospital Chinese Academy of Medical Sciences &amp; Peking Union Medical College  Tianjin China"},{"name":"Tianjin Institute of Health Science  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunlong","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology &amp; 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