ArticleBlood advances2020
Genomic heterogeneity in core-binding factor acute myeloid leukemia and its clinical implication.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 71 citations in OpenAlex.
- Trial
- Genomic landscape of patients with FLT3-mutated acute myeloid leukemia (AML) treated within the CALGB 10603/RATIFY trial.Leukemia · 2022Trial
- Prognostic Impact of Sequential Measurable Residual Disease andAnnals of laboratory medicine · 2026Observational
- Article
- Genetic alterations and measurable residual disease in core binding factor acute myeloid leukemia.Leukemia · 2026Article
- Characterization of Acute Myeloid Leukemia With t(16;21) Translocation: Cytogenetic, Molecular, and Immunophenotypic Findings.World journal of oncology · 2026Article
- Construction of a predictive model based on the risk of relapse after cytarabine consolidation therapy in acute myeloid leukemia patients.The oncologist · 2026Article
- Fusion-specific co-mutational architecture and treatment-response associations in pediatric core-binding factor acute myeloid leukemia: a multicenter exome-profiled cohort.Frontiers in oncology · 2026Article
- Resolving intra-tumor heterogeneity and clonal evolution of core-binding factor acute myeloid leukemia patients with single-cell resolution.Experimental hematology & oncology · 2025Article
- Clinical characteristics and therapeutic determinants ofHaematologica · 2025Article
- PredictingiScience · 2025Article
- Mastocytosis.Nature reviews. Disease primers · 2025Review
- Article
- Genetic abnormalities predict outcomes in patients with core binding factor acute myeloid leukemia.Annals of hematology · 2025Article
- Molecular genetics profiling of core-binding factor acute myeloid leukemia in pediatrics.Therapeutic advances in hematology · 2025Review
- Genomic profiles and outcomes in de novo versus therapy-related core binding factor AML.Blood cancer journal · 2024Article
- Multiomic analysis identifies a high-risk subgroup that predicts poor prognosis in t(8;21) acute myeloid leukemia.Blood cancer journal · 2024Article
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
- The Clonal Hematopoiesis-associated GenebioRxiv : the preprint server for biology · 2024Article
- Prognostic implications of ΔNp73/TAp73 expression ratio in core-binding factor acute myeloid leukemia.Blood cancer journal · 2024Article
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Authors and funding
26 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Core-binding factor (CBF) acute myeloid leukemia (AML) encompasses AML with inv(16)(p13.1q22) and AML with t(8;21)(q22;q22.1). Despite sharing a common pathogenic mechanism involving rearrangements of the CBF transcriptional complex, there is growing evidence for considerable genotypic heterogeneity. We comprehensively characterized the mutational landscape of 350 adult CBF-AML [inv(16): n = 160, t(8;21): n = 190] performing targeted sequencing of 230 myeloid cancer-associated genes. Apart from common mutations in signaling genes, mainly NRAS, KIT, and FLT3, both CBF-AML entities demonstrated a remarkably diverse pattern with respect to the underlying cooperating molecular events, in particular in genes encoding for epigenetic modifiers and the cohesin complex. In addition, recurrent mutations in novel collaborating candidate genes such as SRCAP (5% overall) and DNM2 (6% of t(8;21) AML) were identified. Moreover, aberrations altering transcription and differentiation occurred at earlier leukemic stages and preceded mutations impairing proliferation. Lasso-penalized models revealed an inferior prognosis for t(8;21) AML, trisomy 8, as well as FLT3 and KIT exon 17 mutations, whereas NRAS and WT1 mutations conferred superior prognosis. Interestingly, clonal heterogeneity was associated with a favorable prognosis. When entering mutations by functional groups in the model, mutations in genes of the methylation group (ie, DNMT3A, TET2) had a strong negative prognostic impact.
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