ArticleNature communications2025
Molecular and pharmacological heterogeneity of ETV6::RUNX1 acute lymphoblastic leukemia.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- Article
- The clinical relevance of RAS pathway gene mutations in childhood B-cell acute lymphoblastic leukemia.Annals of hematology · 2026Article
- Chromosome 15q deletions confer inferior outcomes among children with ETV6::RUNX1 B-cell acute lymphoblastic leukemia.Blood advances · 2026Article
- CD33 expression combined with D15-MRD positivity identifies poor prognosis in children with ETV6::RUNX1-positive ALL.Annals of hematology · 2026Article
- The novel ETV6::RARA fusion gene, identified in acute promyelocytic leukemia, is sensitive to invitro all-tans retinoic acid and arsenic trioxide administrations.Annals of hematology · 2026Article
- Article
- Single-center analysis of relapse risk factors and prognosis in 256 cases of ETV6::RUNX1-positive pediatric acute lymphoblastic leukemia.BMC pediatrics · 2026Article
- ELDA: real-time functional drug profiling in acute lymphoblastic leukemia.Frontiers in oncology · 2026Article
- Review
- Treatment-related mutagenic processes in acute lymphoblastic leukemia.Haematologica · 2025Review
- Article
- Error Reduction in Leukemia Machine Learning Classification With Conformal Prediction.JCO clinical cancer informatics · 2025Article
- Harnessing Macrophages in Cancer Therapy: from Immune Modulators to Therapeutic Targets.International journal of biological sciences · 2025Review
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Authors and funding
27 authors.
Funding
Abstract
ETV6::RUNX1 is the most common fusion gene in childhood acute lymphoblastic leukemia (ALL) associated with favorable prognosis, but the optimal therapy for this subtype remains unclear. Profiling the genomic and pharmacological landscape of 194 pediatric ETV6::RUNX1 ALL cases, we uncover two transcriptomic clusters, C1 (61%) and C2 (39%). Compared to C1, the C2 subtype features higher white blood cell counts and younger age at diagnosis, as well as better early treatment responses. Pharmacologically, C2 is more sensitive to thiopurines and prednisolone, partially explained by the enrichment of PAX5 deletions. Re-introducing PAX5 in ETV6::RUNX1 ALL of the C2 subtype converts its gene expression and drug resistance profile to C1, with partial blockade of G1 to S transition mediated by CDK6 expression. Our results point to molecular heterogeneity within ETV6::RUNX1 ALL linked to divergent drug responses, providing insights into the pathogenesis and therapeutic vulnerability of this common pediatric ALL subtype.
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