{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T22:18:23Z","timestamp":1775341103929,"version":"3.50.1"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,11,25]],"date-time":"2025-11-25T00:00:00Z","timestamp":1764028800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2025,11,25]],"date-time":"2025-11-25T00:00:00Z","timestamp":1764028800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100002794","name":"Cancerfonden","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002794","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004047","name":"Karolinska Institutet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004047","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007232","name":"Radiumhemmets Forskningsfonder","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100007232","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2026,2]]},"abstract":"Summary<\/jats:title>\n \n To explore the relation between disease characteristics, comorbidities, mutations and overall survival (OS) in chronic myelomonocytic leukaemia (CMML), we collected data from a population\u2010based cohort of 149 consecutive patients.\n TET2<\/jats:italic>\n mutation (\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n ) was associated with higher haemoglobin, less leucocytosis and longer OS compared to no\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n (\n TET2<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n ), despite patients being significantly older. Patients with multihit\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n had the most favourable outcome (HR 0.55, CI 0.35\u20130.88,\n p<\/jats:italic>\n \u2009<\u20090.05). Multihit\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n was associated with lower lactate dehydrogenase and less monocytosis, indicating multihit\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n as a separate disease entity. Autoimmune disease (AID) was present in 33.6% of patients, with no association to any mutations. In multivariable analysis, the number of\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n was demonstrated to be an independent factor associated with improved OS, and\n RUNX1<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n , myeloproliferative CMML (CMML\u2010MP), ECOG >0 and transfusion dependence remained significant adverse factors. Internal validation including cross\u2010validation and correction for optimism consistently demonstrated that a prognostic model containing the number of\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n ,\n RUNX1<\/jats:italic>\n , CMML\u2010MP, ECOG >0 and transfusion dependence showed better calibration, discrimination and overall performance than CPSS\u2010Mol in predicting OS. Importantly, the addition of\n TET2<\/jats:italic>\n mutation status to CPSS\u2010Mol also improved the CPSS\u2010Mol score performance. Taken together,\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n status, especially multihit\n TET2<\/jats:italic>\n \n MT<\/jats:italic>\n <\/jats:sup>\n , defines a specific CMML phenotype and should be considered in future prognostic scores.\n <\/jats:p>","DOI":"10.1111\/bjh.70264","type":"journal-article","created":{"date-parts":[[2025,11,25]],"date-time":"2025-11-25T08:57:21Z","timestamp":1764061041000},"page":"514-523","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Comorbidities and mutations including single\u2010 and multihit\n TET2<\/i>\n mutations in relation to outcome in chronic myelomonocytic leukaemia\u2014A population\u2010based study"],"prefix":"10.1111","volume":"208","author":[{"given":"Matilda Kjellander","family":"Kynning","sequence":"first","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ebba","family":"Westerberg","sequence":"additional","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Linda","family":"Forsell","sequence":"additional","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria","family":"Creignou","sequence":"additional","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"},{"name":"ME Center for Clinical Cancer Studies Karolinska University Hospital Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel Moreno","family":"Berggren","sequence":"additional","affiliation":[{"name":"Hematology Unit Akademiska University Hospital Stockholm Sweden"},{"name":"Department of Medical Sciences, Section of Hematology Uppsala University Uppsala Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bianca","family":"Tesi","sequence":"additional","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"},{"name":"Department of Clinical Genetics and Genomics Karolinska University Hospital Stockholm Sweden"},{"name":"Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elsa","family":"Bernard","sequence":"additional","affiliation":[{"name":"Institut Gustave Roussy Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elli","family":"Papaemmanuil","sequence":"additional","affiliation":[{"name":"Memorial Sloan Kettering Cancer Center New York New York USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuhito","family":"Nannya","sequence":"additional","affiliation":[{"name":"Department of Hematology\/Oncology Research Hospital, The Institute of Medical Science tUniversity of Tokyo Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucia Cavelier","family":"Franco","sequence":"additional","affiliation":[{"name":"Department of Clinical Genetics and Genomics Karolinska University Hospital Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Davide","family":"Valentini","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine (LabMed) and Center for Bioinformatics and Biostatistics (CBB) Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eva Hellstr\u00f6m","family":"Lindberg","sequence":"additional","affiliation":[{"name":"HERM, Department of Medicine Karolinska Institutet Stockholm Sweden"},{"name":"ME Hematology Karolinska University Hospital Stockholm 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