{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T02:27:25Z","timestamp":1787624845657,"version":"build-2736575974"},"reference-count":38,"publisher":"American Society of Hematology","issue":"6","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,3,25]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Patients with essential thrombocythemia (ET) have a chronic evolution with a risk of hematologic transformation associated with a dismal outcome. Because patients with resistance or intolerance have adverse prognosis, it is important to identify which patient will respond to first-line treatment. We, therefore, aim to describe the association between additional mutations and response to first-line treatment in patients with ET. In this retrospective study, we analyzed the molecular landscape of 121 ET patients first-line treated with hydroxyurea (HU; n\u00a0=\u00a086) or pegylated interferon (peg-IFN; n\u00a0=\u00a035). Patients undergoing peg-IFN therapy were younger and had higher proportion of low and very low risk of thrombosis recurrence. A total of 62 patients (51%) had \u22651 additional mutations at diagnosis. At 12\u00a0months of treatment, 75 patients (62%) achieved complete response (CR), 37 (31%) partial response, and 7 (6%) no response. The presence of at least 1 additional mutation at diagnosis was associated with not achieving CR (hazard ratio [HR], 0.65; P\u00a0=\u00a0.038), whereas treatment with peg-IFN was associated with higher CR (HR, 2.00; P\u00a0=\u00a0.002). The number of additional mutations at diagnosis was associated with hematologic progressions (P\u00a0&amp;lt; .0001). None of the patients receiving peg-IFN therapy progressed to myelofibrosis, whereas 16 of 86 patients (19%) treated with HU developed secondary myelofibrosis. In conclusion, our results suggest that the presence of at least 1 additional mutation at diagnosis is associated with failure to achieve CR and also with an increased risk of hematologic evolution.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/bloodadvances.2024014791","type":"journal-article","created":{"date-parts":[[2025,1,16]],"date-time":"2025-01-16T20:48:48Z","timestamp":1737060528000},"page":"1303-1311","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":4,"title":["Relationship between additional mutations at diagnosis and treatment response in patients with essential thrombocythemia"],"prefix":"10.1182","volume":"9","author":[{"given":"Carole","family":"Mosnier","sequence":"first","affiliation":[{"name":"1Univ Angers, Nantes Universit\u00e9, CHU Angers, INSERM, CNRS, CRCI2NA, Angers, France"},{"name":"2Maladies du Sang, CHU d'Angers, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Bellal","sequence":"additional","affiliation":[{"name":"3Service de Pathologie, Univ Angers, CHU Angers, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7933-8626","authenticated-orcid":false,"given":"Laurane","family":"Cottin","sequence":"additional","affiliation":[{"name":"1Univ Angers, Nantes Universit\u00e9, CHU Angers, INSERM, CNRS, CRCI2NA, Angers, France"},{"name":"4Laboratoire d'H\u00e9matologie, CHU Angers, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7oise","family":"Boyer","sequence":"additional","affiliation":[{"name":"2Maladies du Sang, CHU d'Angers, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9218-7076","authenticated-orcid":false,"given":"Sandrine","family":"Lemoine","sequence":"additional","affiliation":[{"name":"1Univ Angers, Nantes Universit\u00e9, CHU Angers, INSERM, CNRS, CRCI2NA, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0849-4071","authenticated-orcid":false,"given":"Am\u00e9lie","family":"Bachelot","sequence":"additional","affiliation":[{"name":"4Laboratoire d'H\u00e9matologie, CHU Angers, Angers, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0198-8826","authenticated-orcid":false,"given":"Joris","family":"Argentin","sequence":"additional","affiliation":[{"name":"4Laboratoire d'H\u00e9matologie, CHU Angers, Angers, 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