{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T08:53:18Z","timestamp":1790931198696,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T00:00:00Z","timestamp":1783036800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T00:00:00Z","timestamp":1783036800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004398","name":"Mitsubishi Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004398","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017682","name":"Japanese Society of Hematology","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017682","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007451","name":"Cell Science Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007451","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Splicing factor (SF) mutations are recurrent driver alterations in myeloid neoplasms and also represent a distinctive class of mutations in clonal hematopoiesis (CH), an age\u2010associated expansion of hematopoietic clones carrying somatic driver mutations. SF\u2010mutant CH is characterized by relatively late emergence and accelerated clonal expansion in older individuals. This review summarizes current knowledge of the genetic features and clonal dynamics of SF\u2010mutant CH. We discuss disease\u2010associated molecular consequences of SF mutations, including dysregulation of innate immune and inflammatory signaling, R\u2010loop accumulation associated with replication stress, altered stress granule dynamics, impaired minor intron splicing, and cooperative genetic interactions. We further consider candidate mechanisms that may contribute to age\u2010dependent selection of SF\u2010mutant clones during CH, including attenuated interferon responsiveness and telomere\u2010dependent changes in replicative fitness. Together, current evidence highlights the unique biology of SF\u2010mutant CH and the unresolved mechanisms underlying its preferential expansion in older individuals. Clarifying these mechanisms may improve risk stratification, inform early\u2010intervention strategies, and advance our understanding of age\u2010associated clonal evolution and leukemogenesis.<\/jats:p>","DOI":"10.1111\/cas.70461","type":"journal-article","created":{"date-parts":[[2026,7,4]],"date-time":"2026-07-04T00:01:08Z","timestamp":1783123268000},"page":"2609-2618","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Splicing Factor Mutations in Clonal Hematopoiesis and Progression to Myeloid Neoplasms"],"prefix":"10.1111","volume":"117","author":[{"given":"Yang","family":"Lyu","sequence":"first","affiliation":[{"name":"Division of Hematology and Tumor Biology, Institute of Medical Science The University of Tokyo  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yutong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Hematology and Tumor Biology, Institute 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