ArticleOncogene2003
Identification of RUNX1/AML1 as a classical tumor suppressor gene.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- 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
- A phase 1 study of orally administered 5-fluoro-2'-deoxycytidine with tetrahydrouridine in patients with refractory solid tumors.Cancer chemotherapy and pharmacology · 2025Article
- Runx1 promotes the development of glioma cells by regulating JAK-STAT signalling pathway.Archives of medical science : AMS · 2022Article
- RUNX1 Upregulates CENPE to Promote Leukemic Cell Proliferation.Frontiers in molecular biosciences · 2021Article
- Runx1 promotes scar deposition and inhibits myocardial proliferation and survival during zebrafish heart regeneration.Development (Cambridge, England) · 2020Article
- Distinct association of RUNX family expression with genetic alterations and clinical outcome in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2020Article
- Uncovering missed indels by leveraging unmapped reads.Scientific reports · 2019Article
- Expression levels of the runt-related transcription factor 1 and 3 genes in the development of acute myeloid leukemia.Oncology letters · 2018Article
- Relationship between RUNX1 and AXIN1 in ER-negative versus ER-positive Breast Cancer.Cell cycle (Georgetown, Tex.) · 2017Article
- High expression of RUNX1 is associated with poorer outcomes in cytogenetically normal acute myeloid leukemia.Oncotarget · 2016Article
- Article
- Genomic Profile of Chronic Lymphocytic Leukemia in Korea Identified by Targeted Sequencing.PloS one · 2016Article
- The RUNX1-PU.1 axis in the control of hematopoiesis.International journal of hematology · 2015Review
- Two novel RUNX1 mutations in a patient with congenital thrombocytopenia that evolved into a high grade myelodysplastic syndrome.Leukemia research reports · 2015Article
- Article
- Somatic retrotransposition in human cancer revealed by whole-genome and exome sequencing.Genome research · 2014Article
- Characterization of changes in gene expression and biochemical pathways at low levels of benzene exposure.PloS one · 2014Article
- Essential role for Dnmt1 in the prevention and maintenance of MYC-induced T-cell lymphomas.Molecular and cellular biology · 2013Article
- Review
- TdT expression in acute myeloid leukemia with minimal differentiation is associated with distinctive clinicopathological features and better overall survival following stem cell transplantation.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Based on our previous results indicating the presence of a tumor suppressor gene (TSG), chromosome 21 was analysed for loss of heterozygosity (LOH) in 18 patients with acute myeloid leukemia (17, AML-M0; one, AML-M1). Allelotyping at polymorphic loci was performed on purified material, allowing unequivocal detection of allelic loss and homozygous deletions. Six AML-M0 patients shared a common region of LOH harboring a single gene: RUNX1 (AML1), the most frequent site of translocations in acute leukemia and a well-known fusion oncogene. Fluorescence in situ hybridization allowed the identification of deletions with breakpoints within RUNX1 in two patients as the cause of LOH. In the four others the LOH pattern and the presence of two karyotypically normal chromosomes 21 were in line with mitotic recombination. Further molecular and cytogenetic analyses showed that this caused homozygosity of primary RUNX1 mutations: two point mutations, a partial deletion and, most significantly, a complete deletion of RUNX1. These findings identify RUNX1 as a classical TSG: both alleles are mutated or absent in cancer cells from four of the 17 AML-M0 patients examined. In contrast to AML-M0, the AML-M1 patient was trisomic for chromosome 21 and has two mutated and one normal RUNX1 allele, suggesting that the order of mutagenic events leading to leukemia may influence the predominant tumor type.
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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.