<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(15)</volume><submitter>Vasseur L</submitter><pubmed_abstract>Whether the LSC17 gene expression can improve risk stratification in the context of next generation sequencing-based risk stratification and measurable residual disease (MRD) in patients with intensively treated AML has not been explored. We analyzed LSC17 in 504 adult patients prospectively treated in the ALFA-0702 trial. RUNX1 or TP53 mutations were associated with higher LSC1 scores while CEBPA and NPM1 mutations were associated with lower scores. Patients with high LSC17 scores had a lower rate of complete response (CR) in a multivariable analysis (odds ratio, 0.41; P = .0007), accounting for European LeukemiaNet 2022 (ELN22), age, and white blood cell count (WBC). LSC17-high status was associated with shorter overall survival (OS) (3-year OS: 70.0% vs 52.7% in patients with LSC17-low </pubmed_abstract><journal>Blood advances</journal><pagination>4024-4034</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10410128</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>LSC17 score complements genetics and measurable residual disease in acute myeloid leukemia: an ALFA study.</pubmed_title><pmcid>PMC10410128</pmcid><pubmed_authors>Lebon D</pubmed_authors><pubmed_authors>Dombret H</pubmed_authors><pubmed_authors>Heiblig M</pubmed_authors><pubmed_authors>Celli-Lebras K</pubmed_authors><pubmed_authors>Berthon C</pubmed_authors><pubmed_authors>Recher C</pubmed_authors><pubmed_authors>Fenwarth L</pubmed_authors><pubmed_authors>Duployez N</pubmed_authors><pubmed_authors>Lambert J</pubmed_authors><pubmed_authors>Dumas PY</pubmed_authors><pubmed_authors>Figeac M</pubmed_authors><pubmed_authors>Cheok M</pubmed_authors><pubmed_authors>Terre C</pubmed_authors><pubmed_authors>Itzykson R</pubmed_authors><pubmed_authors>Lemasle E</pubmed_authors><pubmed_authors>de Botton S</pubmed_authors><pubmed_authors>Preudhomme C</pubmed_authors><pubmed_authors>Villenet C</pubmed_authors><pubmed_authors>Vasseur L</pubmed_authors></additional><is_claimable>false</is_claimable><name>LSC17 score complements genetics and measurable residual disease in acute myeloid leukemia: an ALFA study.</name><description>Whether the LSC17 gene expression can improve risk stratification in the context of next generation sequencing-based risk stratification and measurable residual disease (MRD) in patients with intensively treated AML has not been explored. We analyzed LSC17 in 504 adult patients prospectively treated in the ALFA-0702 trial. RUNX1 or TP53 mutations were associated with higher LSC1 scores while CEBPA and NPM1 mutations were associated with lower scores. Patients with high LSC17 scores had a lower rate of complete response (CR) in a multivariable analysis (odds ratio, 0.41; P = .0007), accounting for European LeukemiaNet 2022 (ELN22), age, and white blood cell count (WBC). LSC17-high status was associated with shorter overall survival (OS) (3-year OS: 70.0% vs 52.7% in patients with LSC17-low </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2026-05-28T13:05:23.157Z</modification><creation>2024-12-04T05:25:29.335Z</creation></dates><accession>S-EPMC10410128</accession><cross_references><pubmed>37205853</pubmed><doi>10.1182/bloodadvances.2023010155</doi></cross_references></HashMap>