{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Saygin C"],"funding":["Cancer Research Foundation","NHLBI NIH HHS","NCI NIH HHS","National Institutes of Health","Elsa U. Pardee Foundation","Prevent Cancer Foundation","Leukemia and Lymphoma Society"],"pagination":["164-179"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11061587"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(3)"],"pubmed_abstract":["Myeloid neoplasms arise from preexisting clonal hematopoiesis (CH); however, the role of CH in the pathogenesis of acute lymphoblastic leukemia (ALL) is unknown. We found that 18% of adult ALL cases harbored TP53, and 16% had myeloid CH-associated gene mutations. ALL with myeloid mutations (MyM) had distinct genetic and clinical characteristics, associated with inferior survival. By using single-cell proteogenomic analysis, we demonstrated that myeloid mutations were present years before the diagnosis of ALL, and a subset of these clones expanded over time to manifest as dominant clones in ALL. Single-cell RNA sequencing revealed upregulation of genes associated with cell survival and resistance to apoptosis in B-ALL with MyM, which responds better to newer immunotherapeutic approaches. Th"],"journal":["Blood cancer discovery"],"pubmed_title":["Acute Lymphoblastic Leukemia with Myeloid Mutations Is a High-Risk Disease Associated with Clonal Hematopoiesis."],"pmcid":["PMC11061587"],"funding_grant_id":["P01CA066996","P50CA206963","P50 CA206963","P01 CA066996","R01HL082945","R01 HL082945","F30 HL162455","K08 CA252174"],"pubmed_authors":["Steidl U","Ebert BL","Wanjari P","Arber DA","Zhang P","Umesh Nagalakshmi S","Larson RA","Godley LA","Stock W","Saygin C","Lager AM","Odenike OM","Gibson CJ","Wang P","Stauber J","Weeks LD","Munshi NC","Cheng JX","Aldoss I","Patel AA","Marcucci G","Knepper TC","Segal JP","Eisfelder BJ","Shah BD","Luskin MR","Lapalombella R","Sperling AS","Greally JM","Venkataraman G","Gharghabi M","Jayaram S","Fitzpatrick C","Gurbuxani S","Bohorquez O"],"additional_accession":[]},"is_claimable":false,"name":"Acute Lymphoblastic Leukemia with Myeloid Mutations Is a High-Risk Disease Associated with Clonal Hematopoiesis.","description":"Myeloid neoplasms arise from preexisting clonal hematopoiesis (CH); however, the role of CH in the pathogenesis of acute lymphoblastic leukemia (ALL) is unknown. We found that 18% of adult ALL cases harbored TP53, and 16% had myeloid CH-associated gene mutations. ALL with myeloid mutations (MyM) had distinct genetic and clinical characteristics, associated with inferior survival. By using single-cell proteogenomic analysis, we demonstrated that myeloid mutations were present years before the diagnosis of ALL, and a subset of these clones expanded over time to manifest as dominant clones in ALL. Single-cell RNA sequencing revealed upregulation of genes associated with cell survival and resistance to apoptosis in B-ALL with MyM, which responds better to newer immunotherapeutic approaches. Th","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-02T18:38:01.404Z","creation":"2025-04-04T00:29:35.064Z"},"accession":"S-EPMC11061587","cross_references":{"pubmed":["38150184"],"doi":["10.1158/2643-3230.BCD-23-0106"]}}