ReviewOncogene2004
Point mutations in the RUNX1/AML1 gene: another actor in RUNX leukemia.
Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
123 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.
- Prognostic Value of RUNX1 Mutations in AML: A Meta-AnalysisAsian Pacific journal of cancer prevention : APJCP · 2018Pooled it
- RUNX1 mutations are associated with poor outcome in younger and older patients with cytogenetically normal acute myeloid leukemia and with distinct gene and MicroRNA expression signatures.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012Trial
- Immunophenotypic, Genetic, and Clinical Features Associated With RUNX1 Mutation in Acute Leukemias and Chronic Myeloid Neoplasms.International journal of laboratory hematology · 2026Article
- Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.MedComm · 2024Review
- RUNX1 targeting AKT3 promotes alveolar hypercoagulation and fibrinolytic inhibition in LPS induced ARDS.Respiratory research · 2024Article
- Review
- Runt-related transcription factors in human carcinogenesis: a friend or foe?Journal of cancer research and clinical oncology · 2023Review
- The Therapeutic Potential of a Strategy to Prevent Acute Myeloid Leukemia Stem Cell Reprogramming in Older Patients.International journal of molecular sciences · 2023Review
- RUNX1 mutation has no prognostic significance in paediatric AML: a retrospective study of the AML-BFM study group.Leukemia · 2023Article
- Article
- A critical role of RUNX1 in governing megakaryocyte-primed hematopoietic stem cell differentiation.Blood advances · 2023Article
- Childhood hematopoietic stem cells constitute the permissive window for RUNX1-ETO leukemogenesis.International journal of hematology · 2023Review
- Prolonged generation of multi-lineage blood cells in wild-type animals from pluripotent stem cells.Stem cell reports · 2023Article
- Review
- Muscle Regeneration in Holothurians without the Upregulation of Muscle Genes.International journal of molecular sciences · 2022Article
- Regulome analysis in B-acute lymphoblastic leukemia exposes Core Binding Factor addiction as a therapeutic vulnerability.Nature communications · 2022Article
- Review
- UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.International journal of hematology · 2022Article
- The spectrum of genetic mutations in myelodysplastic syndrome: Should we update prognostication?EJHaem · 2022Review
- Hematopoietic Stem Cell Factors: Their Functional Role in Self-Renewal and Clinical Aspects.Frontiers in cell and developmental biology · 2022Review
63 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RUNX1/AML1 gene is the most frequent target for chromosomal translocation in leukemia. In addition, recent studies have demonstrated point mutations in the RUNX1 gene as another mode of genetic alteration in development of leukemia. Monoallelic germline mutations in RUNX1 result in familial platelet disorder predisposed to acute myelogenous leukemia (FPD/AML). Sporadic point mutations are frequently found in three leukemia entities: AML M0 subtype, MDS-AML, and secondary (therapy-related) MDS/AML. Therapy-related leukemias resulting from anticancer treatments are not uncommon, and the incidence of RUNX1 point mutations appears comparable to the incidence of the t(8;21) AML M2 subtype and the inv(16) AML M4Eo subtype. Half of the point mutations in M0 cases are biallelic, although the frequency varies with ethnicity. Most of the RUNX1 mutations are clustered in the Runt domain and result in defective DNA binding but active beta-subunit binding, which is consistent with three-dimensional structural findings and may explain the dominant inhibitory effects. Unlike the classical tumor suppressor genes requiring biallelic inactivation, haploinsufficient RUNX1 is apparently leukemogenic. However, RUNX1 abnormalities per se are insufficient to cause full-blown leukemia. Intensive investigation of cooperating genetic alterations should elucidate leukemic mechanisms.
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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.