{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:35:24Z","timestamp":1786977324336,"version":"build-2736575974"},"reference-count":49,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,2,17]],"date-time":"2023-02-17T00:00:00Z","timestamp":1676592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Medicine"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Myeloid neoplasms (MN) tend to relapse and deteriorate. Exploring the genomic mutation landscape of MN using next\u2010generation sequencing (NGS) is a great measure to clarify the mechanism of oncogenesis and progression of MN.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This multicenter retrospective study investigated 303 patients with MN using NGS from 2019 to 2021. The characteristics of the mutation landscape in the MN subgroups and the clinical value of gene variants were analyzed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At least one mutation was detected in 88.11% of the patients (267\/303).\n                      <jats:italic>TET2<\/jats:italic>\n                      was the most common mutation in the cohort, followed by\n                      <jats:italic>GATA2, ASXL1, FLT3, DNMT3A<\/jats:italic>\n                      , and\n                      <jats:italic>TP53<\/jats:italic>\n                      . Among patients with myeloid leukemia (ML), multivariate analysis showed that patients aged \u226560\u2009years had lower overall survival (OS,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a00.004). Further analysis showed\n                      <jats:italic>TET2, NPM1, SRSF2<\/jats:italic>\n                      , and\n                      <jats:italic>IDH1<\/jats:italic>\n                      gene mutations, and epigenetic genes (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.050) presented significantly higher frequency in older patients. In patients with myelodysplastic syndrome (MDS) and myelodysplastic neoplasms (MPN), univariate analysis showed that\n                      <jats:italic>BCORL1<\/jats:italic>\n                      had a significant impact on OS (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a00.040); however, in multivariate analysis, there were no factors significantly associated with OS. Differential analysis of genetic mutations showed\n                      <jats:italic>FLT3, TP53, MUC16, SRSF2<\/jats:italic>\n                      , and\n                      <jats:italic>KDM5A<\/jats:italic>\n                      mutated more frequently (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.050) in secondary acute myeloid leukemia (s\u2010AML) than in MDS and MPN.\n                      <jats:italic>TP53, U2AF1, SRSF2<\/jats:italic>\n                      , and\n                      <jats:italic>KDM5A<\/jats:italic>\n                      were mutated more frequently (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.050) in s\u2010AML than in primary AML.\n                      <jats:italic>KDM5A<\/jats:italic>\n                      was observed to be restricted to patients with s\u2010AML in this study, and only co\u2010occurred with\n                      <jats:italic>MUC16<\/jats:italic>\n                      and\n                      <jats:italic>TP53<\/jats:italic>\n                      (2\/2, 100%). Another mutation was\n                      <jats:italic>MUC16<\/jats:italic>\n                      , and its co\u2010occurrence pattern differed between s\u2010AML and AML. MUC16 mutations co\u2010occurred with\n                      <jats:italic>KDM5A<\/jats:italic>\n                      and\n                      <jats:italic>TP53<\/jats:italic>\n                      in 66.7% (2\/3) of patients with s\u2010AML and co\u2010occurred with\n                      <jats:italic>CEBPA<\/jats:italic>\n                      in 100% (4\/4) of patients with AML.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results demonstrate different genomic mutation patterns in the MN subgroups and highlight the clinical value of genetic variants.<\/jats:p>\n                  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