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               <dc:title>Outcomes and molecular profile of oligomonocytic CMML support its consideration as the first stage in the CMML continuum</dc:title>
               <dc:creator>Calvo González, Xavier</dc:creator>
               <dc:creator>Roman-Bravo, David</dc:creator>
               <dc:creator>García Gisbert, Nieves, 1994-</dc:creator>
               <dc:creator>Rodriguez-Sevilla, Juan José</dc:creator>
               <dc:creator>García-Ávila, Sara</dc:creator>
               <dc:creator>Florensa Brichs, Lourdes</dc:creator>
               <dc:creator>Gibert Fernandez, Joan, 1988-</dc:creator>
               <dc:creator>Fernández Rodríguez, M. Concepción</dc:creator>
               <dc:creator>Salido Galeote, Marta</dc:creator>
               <dc:creator>Puiggros Metje, Anna Maria</dc:creator>
               <dc:creator>Espinet Solà, Blanca</dc:creator>
               <dc:creator>Colomo Saperas, Luis Alberto</dc:creator>
               <dc:creator>Bellosillo Paricio, Beatriz</dc:creator>
               <dc:creator>Ferrer, Ana</dc:creator>
               <dc:creator>Arenillas Rocha, Leonor</dc:creator>
               <dc:subject>Leucèmia</dc:subject>
               <dc:subject>Leucèmia mieloide</dc:subject>
               <dc:description>atients with oligomonocytic chronic myelomonocytic leukemia (OM-CMML) are currently classified according to the 2017 World Health Organization myelodysplastic syndromes classification. However, recent data support considering OM-CMML as a specific subtype of chronic myelomonocytic leukemia (CMML), given their similar clinical, genomic, and immunophenotypic profiles. The main purpose of our study was to provide survival outcome data of a well-annotated series of 42 patients with OM-CMML and to compare them to 162 patients with CMML, 120 with dysplastic type (D-CMML), and 42 with proliferative type (P-CMML). OM-CMML had significantly longer overall survival (OS) and acute myeloid leukemia-free survival than did patients with CMML, considered as a whole group, and when compared with D-CMML and P-CMML. Moreover, gene mutations associated with increased proliferation (ie, ASXL1 and RAS-pathway mutations) were identified as independent adverse prognostic factors for OS in our series. We found that at a median follow-up of 53.47 months, 29.3% of our patients with OM-CMML progressed to D-CMML, and at a median follow-up of 46.03 months, 28.6% of our D-CMML group progressed to P-CMML. These data support the existence of an evolutionary continuum of OM-CMML, D-CMML, and P-CMML. In this context, we observed that harboring more than 3 mutated genes, carrying ASXL1 mutations, and a peripheral blood monocyte percentage &amp;gt;20% significantly predicted a shorter time of progression of OM-CMML into overt CMML. These variables were also detected as independent adverse prognostic factors for OS in OM-CMML. These data support the consideration of OM-CMML as the first evolutionary stage within the proliferative continuum of CMML.</dc:description>
               <dc:date>2022-10-07T06:28:17Z</dc:date>
               <dc:date>2022-10-07T06:28:17Z</dc:date>
               <dc:date>2022</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:rights>Copyright © 2022 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) http://creativecommons.org/licenses/by-nc-nd/4.0/legalcode, permitting only noncommercial, nonderivative use with attribution. All other rights reserved.</dc:rights>
               <dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/legalcode</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>American Society of Hematology</dc:publisher>
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