<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-14T03:54:03Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/16136" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/16136</identifier><datestamp>2024-11-30T00:30:43Z</datestamp><setSpec>com_20.500.12105_2173</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19597</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Ayala, Rosa</subfield>
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      <subfield code="a">Carreño-Tarragona, Gonzalo</subfield>
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      <subfield code="a">Barragán, Eva</subfield>
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      <subfield code="a">Boluda, Blanca</subfield>
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      <subfield code="a">Larráyoz, María J</subfield>
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      <subfield code="a">Chillón, María Carmen</subfield>
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      <subfield code="a">Carrillo-Cruz, Estrella</subfield>
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      <subfield code="a">Bilbao, Cristina</subfield>
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      <subfield code="a">Sánchez-García, Joaquín</subfield>
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      <subfield code="a">Bernal, Teresa</subfield>
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      <subfield code="a">Martinez-Cuadron, David</subfield>
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      <subfield code="a">Gil, Cristina</subfield>
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      <subfield code="a">Serrano, Josefina</subfield>
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      <subfield code="a">Rodriguez-Medina, Carlos</subfield>
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      <subfield code="a">Bergua, Juan</subfield>
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      <subfield code="a">Pérez-Simón, José A</subfield>
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      <subfield code="a">Calbacho, María</subfield>
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      <subfield code="a">Alonso-Domínguez, Juan M</subfield>
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      <subfield code="a">Labrador, Jorge</subfield>
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      <subfield code="a">Tormo, Mar</subfield>
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      <subfield code="a">Amigo, Maria Luz</subfield>
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      <subfield code="a">Herrera-Puente, Pilar</subfield>
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      <subfield code="a">Rapado, Inmaculada</subfield>
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      <subfield code="a">Sargas, Claudia</subfield>
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      <subfield code="a">Vazquez, Iria</subfield>
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      <subfield code="a">Calasanz, María J</subfield>
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      <subfield code="a">Gomez-Casares, Teresa</subfield>
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      <subfield code="a">García-Sanz, Ramón</subfield>
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      <subfield code="a">Sanz, Miguel A</subfield>
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      <subfield code="a">Martinez-Lopez, Joaquin</subfield>
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      <subfield code="a">Montesinos, Pau</subfield>
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      <subfield code="c">2022-11-24</subfield>
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      <subfield code="a">FLT3−ITD results in a poor prognosis in terms of overall survival (OS) and relapse-free survival (RFS) in acute myeloid leukemia (AML). However, the prognostic usefulness of the allelic ratio (AR) to select post-remission therapy remains controversial. Our study focuses on the prognostic impact of FLT3−ITD and its ratio in a series of 2901 adult patients treated intensively in the pre-FLT3 inhibitor era and reported in the PETHEMA registry. A total of 579 of these patients (20%) harbored FLT3−ITD mutations. In multivariate analyses, patients with an FLT3−ITD allele ratio (AR) of >0.5 showed a lower complete remission (CR rate) and OS (HR 1.47, p = 0.009), while AR > 0.8 was associated with poorer RFS (HR 2.1; p &lt; 0.001). Among NPM1/FLT3−ITD-mutated patients, median OS gradually decreased according to FLT3−ITD status and ratio (34.3 months FLT3−ITD-negative, 25.3 months up to 0.25, 14.5 months up to 0.5, and 10 months ≥ 0.5, p &lt; 0.001). Post-remission allogeneic transplant (allo-HSCT) resulted in better OS and RFS as compared to auto-HSCT in NPM1/FLT3−ITD-mutated AML regardless of pre-established AR cutoff (≤0.5 vs. >0.5). Using the maximally selected log-rank statistics, we established an optimal cutoff of FLT3−ITD AR of 0.44 for OS, and 0.8 for RFS. We analyzed the OS and RFS according to FLT3−ITD status in all patients, and we found that the group of FLT3−ITD-positive patients with AR &lt; 0.44 had similar 5-year OS after allo-HSCT or auto-HSCT (52% and 41%, respectively, p = 0.86), but worse RFS after auto-HSCT (p = 0.01). Among patients with FLT3−ITD AR > 0.44, allo-HSCT was superior to auto-HSCT in terms of OS and RFS. This study provides more evidence for a better characterization of patients with AML harboring FLT3−ITD mutations.</subfield>
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      <subfield code="a">Cancers (Basel). 2022;14(23):5799.</subfield>
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      <subfield code="a">10.3390/cancers14235799</subfield>
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      <subfield code="a">2072-6694</subfield>
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      <subfield code="a">Cancers</subfield>
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      <subfield code="a">36497281</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/16136</subfield>
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      <subfield code="a">FLT3-ITD mutation and ratio</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">real-world outcomes</subfield>
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      <subfield code="a">ACUTE MYELOID LEUKEMIA</subfield>
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      <subfield code="a">PROGNOSIS</subfield>
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      <subfield code="a">SURVIVAL</subfield>
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   <datafield ind2="0" ind1="0" tag="245">
      <subfield code="a">Impact of FLT3-ITD Mutation Status and Its Ratio in a Cohort of 2901 Patients Undergoing Upfront Intensive Chemotherapy: A PETHEMA Registry Study.</subfield>
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