<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>143(14)</volume><submitter>Bastian L</submitter><pubmed_abstract>&lt;h4>Abstract&lt;/h4>Distinct diagnostic entities within BCR::ABL1-positive acute lymphoblastic leukemia (ALL) are currently defined by the International Consensus Classification of myeloid neoplasms and acute leukemias (ICC): "lymphoid only", with BCR::ABL1 observed exclusively in lymphatic precursors, vs "multilineage", where BCR::ABL1 is also present in other hematopoietic lineages. Here, we analyzed transcriptomes of 327 BCR::ABL1-positive patients with ALL (age, 2-84 years; median, 46 years) and identified 2 main gene expression clusters reproducible across 4 independent patient cohorts. Fluorescence in situ hybridization analysis of fluorescence-activated cell-sorted hematopoietic compartments showed distinct BCR::ABL1 involvement in myeloid cells for these clusters (n = 18/18 vs n = 3/1</pubmed_abstract><journal>Blood</journal><pagination>1391-1398</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11033585</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Developmental trajectories and cooperating genomic events define molecular subtypes of BCR::ABL1-positive ALL.</pubmed_title><pmcid>PMC11033585</pmcid><pubmed_authors>Gokbuget N</pubmed_authors><pubmed_authors>Wittig M</pubmed_authors><pubmed_authors>Bastian L</pubmed_authors><pubmed_authors>Wolgast N</pubmed_authors><pubmed_authors>Hartmann AM</pubmed_authors><pubmed_authors>Zimmermann J</pubmed_authors><pubmed_authors>Neumann M</pubmed_authors><pubmed_authors>Baldus CD</pubmed_authors><pubmed_authors>Haferlach C</pubmed_authors><pubmed_authors>Brandl B</pubmed_authors><pubmed_authors>Das Gupta D</pubmed_authors><pubmed_authors>Chitadze G</pubmed_authors><pubmed_authors>Denker M</pubmed_authors><pubmed_authors>Faul C</pubmed_authors><pubmed_authors>Bruggemann M</pubmed_authors><pubmed_authors>Stelljes M</pubmed_authors><pubmed_authors>Schneller F</pubmed_authors><pubmed_authors>Bendig S</pubmed_authors><pubmed_authors>Schwartz S</pubmed_authors><pubmed_authors>Muller FJ</pubmed_authors><pubmed_authors>Fiedler W</pubmed_authors><pubmed_authors>Beder T</pubmed_authors><pubmed_authors>Steffen B</pubmed_authors><pubmed_authors>Pfeifer H</pubmed_authors><pubmed_authors>Barz MJ</pubmed_authors><pubmed_authors>Iben K</pubmed_authors><pubmed_authors>Harder L</pubmed_authors><pubmed_authors>Bartsch L</pubmed_authors><pubmed_authors>Rohrandt C</pubmed_authors><pubmed_authors>Walter W</pubmed_authors><pubmed_authors>Hansen BT</pubmed_authors><pubmed_authors>Cario G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Developmental trajectories and cooperating genomic events define molecular subtypes of BCR::ABL1-positive ALL.</name><description>&lt;h4>Abstract&lt;/h4>Distinct diagnostic entities within BCR::ABL1-positive acute lymphoblastic leukemia (ALL) are currently defined by the International Consensus Classification of myeloid neoplasms and acute leukemias (ICC): "lymphoid only", with BCR::ABL1 observed exclusively in lymphatic precursors, vs "multilineage", where BCR::ABL1 is also present in other hematopoietic lineages. Here, we analyzed transcriptomes of 327 BCR::ABL1-positive patients with ALL (age, 2-84 years; median, 46 years) and identified 2 main gene expression clusters reproducible across 4 independent patient cohorts. Fluorescence in situ hybridization analysis of fluorescence-activated cell-sorted hematopoietic compartments showed distinct BCR::ABL1 involvement in myeloid cells for these clusters (n = 18/18 vs n = 3/1</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-06-01T09:20:47.097Z</modification><creation>2026-04-08T11:06:20.44Z</creation></dates><accession>S-EPMC11033585</accession><cross_references><pubmed>38153913</pubmed><doi>10.1182/blood.2023021752</doi></cross_references></HashMap>