ArticleBlood cancer discovery2024
Acute Lymphoblastic Leukemia with Myeloid Mutations Is a High-Risk Disease Associated with Clonal Hematopoiesis.
Article in Blood cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Acute lymphoblastic leukemia in patients treated with lenalidomide for multiple myeloma: a safety meta-analysis of randomized controlled trials combined with a retrospective study of the WHO's pharmacovigilance database.Blood cancer journal · 2024Pooled it
- Comparative efficacy and long-term survival of CD19/22 versus CD19 CAR-T immunotherapy in Relapsed/Refractory B-ALL with TP53 alterations.Journal of translational medicine · 2026Trial
- The prognostic role of myeloid-related gene mutations in adult acute lymphoblastic leukemia.Haematologica · 2026Article
- The machine-learning classifier ALLCatchR2 identifies 20 T-ALL subtypes across cohorts and age groups.HemaSphere · 2026Article
- Clonal Hematopoiesis in Colorectal Cancer: Mechanisms and Implications.Cancer medicine · 2026Review
- Mutations in isocitrate dehydrogenase portend a poor prognosis in adult patients with acute lymphoblastic leukemia.Blood advances · 2026Article
- Clonal hematopoiesis dynamics influences long-term outcomes of follicular lymphoma: Results from FIL FOLL12 trial.HemaSphere · 2026Article
- Clinical decisions in clonal hematopoiesis: a contemporary review for clinicians.Haematologica · 2026Review
- Clonal hematopoiesis and its progression to myeloid neoplasms: insights into risk, biology, and therapeutic strategies.Haematologica · 2026Review
- CD19-negative relapse after CAR-T cell therapy: mechanisms of antigen escape and lineage switch.Frontiers in immunology · 2026Review
- Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies.Cancer discovery · 2025Article
- Pediatric T-Lymphoblastic Leukemia With Aberrant B-Cell Marker Expression: A Potential Role for Targeted Therapy.EJHaem · 2025Article
- Article
- Synergistic MDM2-STAT3 Inhibition Demonstrates Strong Anti-Leukemic Efficacy in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Article
- Evolution of clonal hematopoiesis on and off lenalidomide maintenance for multiple myeloma.Leukemia · 2025Article
- Clinical and molecular characterization of TP53-mutant acute lymphoblastic leukemia in adults.Blood cancer journal · 2025Article
- Acute pro-B-cell lymphoblastic leukemia evolving from myelodysplastic neoplasm post cytotoxic therapy: a case report.Haematologica · 2025Article
- The dynamic evolution of lineage switch under CD19 CAR-T treatment in non-KMT2A rearranged B-ALL patients.Leukemia · 2025Article
- CHIP: a clonal odyssey of the bone marrow niche.The Journal of clinical investigation · 2024Review
- "Myeloid" Mutations in ALL Are Not Uncommon: Implications for Etiology and Therapies.Blood cancer discovery · 2024Article
Corrections and comments
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Authors and funding
35 authors at 10 institutions in 1 country.
Funding
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. These findings define ALL with MyM as a high-risk disease that can arise from antecedent CH and offer new mechanistic insights to develop better therapeutic and preventative strategies. SIGNIFICANCE: CH is a precursor lesion for lymphoblastic leukemogenesis. ALL with MyM has distinct genetic and clinical characteristics, associated with adverse survival outcomes after chemotherapy. CH can precede ALL years before diagnosis, and ALL with MyM is enriched with activated T cells that respond to immunotherapies such as blinatumomab. See related commentary by Iacobucci, p. 142.
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