ReviewBlood advances2020
An update on the molecular pathogenesis and potential therapeutic targeting of AML with t(8;21)(q22;q22.1);RUNX1-RUNX1T1.
Review in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.
- Genetic alterations in myeloid sarcoma among acute myeloid leukemia patients: insights from 37 cohort studies and a meta-analysis.Frontiers in oncology · 2024Pooled it
- Pooled it
- Phase II study of dual epigenetic targeting with chidamide and azacitidine in patients with high-risk acute myeloid leukemia after allo-HSCT.Clinical epigenetics · 2025Trial
- Single-cell chromatin profiling reveals relapse-related priming in pediatric acute myeloid leukemia.Life science alliance · 2026Article
- Article
- PKC isoforms in hematopoietic lineages and myeloid/lymphoid leukemias: mechanistic insights and therapeutic prospects.Frontiers in oncology · 2026Review
- Nomogram-based prediction models for clinical outcomes in pediatricFrontiers in oncology · 2026Article
- The Dual Role of RUNX1 in Inflammation-Driven Age-Related Diseases: From Molecular Mechanisms to Clinical Translation.Biomedicines · 2025Review
- Acute Myeloid Leukemia with MYC Amplification on a Ring Chromosome 8.Internal medicine (Tokyo, Japan) · 2025Article
- A novel manganese metabolism- and immune-related prognostic risk model for acute myeloid leukemia.Translational cancer research · 2025Article
- Review
- Observational
- A Novel Approach to Prognostic Factors and Risk Stratification in Pediatric AML: Case Report and Literature Review.International journal of molecular sciences · 2025Review
- t(8;21)AML patients with RUNX1e6::RUNX1T19a splice variant have poor prognosis.Annals of hematology · 2025Article
- PredictingiScience · 2025Article
- Allogeneic stem cell transplantation in de novo core-binding factor acute myeloid leukemia in active disease: a study from the Acute Leukemia Working Party of the European Society for Blood and Marrow Transplantation.Bone marrow transplantation · 2025Article
- Long non-coding RNAs in humans: Classification, genomic organization and function.Non-coding RNA research · 2025Review
- Diagnosis and treatment of AML in the context of WHO and ICC 2022 classifications: Divergent nomenclature converges on common therapies.HemaSphere · 2025Review
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Cellular hierarchy for understanding heterogeneity of acute myeloid leukaemia with t(8;21)/RUNX1-RUNX1T1.Clinical & translational immunology · 2025Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) with t(8;21)(q22;q22.1);RUNX1-RUNX1T1, one of the core-binding factor leukemias, is one of the most common subtypes of AML with recurrent genetic abnormalities and is associated with a favorable outcome. The translocation leads to the formation of a pathological RUNX1-RUNX1T1 fusion that leads to the disruption of the normal function of the core-binding factor, namely, its role in hematopoietic differentiation and maturation. The consequences of this alteration include the recruitment of repressors of transcription, thus blocking the expression of genes involved in hematopoiesis, and impaired apoptosis. A number of concurrent and cooperating mutations clearly play a role in modulating the proliferative potential of cells, including mutations in KIT, FLT3, and possibly JAK2. RUNX1-RUNX1T1 also appears to interact with microRNAs during leukemogenesis. Epigenetic factors also play a role, especially with the recruitment of histone deacetylases. A better understanding of the concurrent mutations, activated pathways, and epigenetic modulation of the cellular processes paves the way for exploring a number of approaches to achieve cure. Potential approaches include the development of small molecules targeting the RUNX1-RUNX1T1 protein, the use of tyrosine kinase inhibitors such as dasatinib and FLT3 inhibitors to target mutations that lead to a proliferative advantage of the leukemic cells, and experimentation with epigenetic therapies. In this review, we unravel some of the recently described molecular pathways and explore potential therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.