ArticleBritish journal of haematology2015
RUNX3 promoter hypermethylation is frequent in leukaemia cell lines and associated with acute myeloid leukaemia inv(16) subtype.
Article in British journal of haematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- The DNA Methylation-Autophagy Axis: A Driver of MSC Fate Imbalance in Skeletal Aging and Osteoporosis.Biology · 2026Review
- Hypomethylating agent monotherapy in core binding factor acute myeloid leukemia: a French multicentric retrospective study.Annals of hematology · 2024Article
- Expression patterns and prognostic value of RUNX genes in kidney cancer.Scientific reports · 2021Article
- Fine particulate matter induces airway inflammation by disturbing the balance between Th1/Th2 and regulation of GATA3 and Runx3 expression in BALB/c mice.Molecular medicine reports · 2021Article
- Runx Transcription Factors in T Cells-What Is Beyond Thymic Development?Frontiers in immunology · 2021Review
- Distinct association of RUNX family expression with genetic alterations and clinical outcome in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2020Article
- Expression ofOncology letters · 2019Article
- Dysregulation of the TOX-RUNX3 pathway in cutaneous T-cell lymphoma.Oncotarget · 2019Article
- Genome-Wide Association Study on Immunoglobulin G Glycosylation Patterns.Frontiers in immunology · 2018Article
- Identification of sequence variants influencing immunoglobulin levels.Nature genetics · 2017Article
- Regulation of miRNA-29c and its downstream pathways in preneoplastic progression of triple-negative breast cancer.Oncotarget · 2017Article
- Inhibition of DNA and Histone Methylation by 5-Aza-2'-Deoxycytidine (Decitabine) and 3-Deazaneplanocin-A on Antineoplastic Action and Gene Expression in Myeloid Leukemic Cells.Frontiers in oncology · 2017Article
- Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.Oncotarget · 2016Review
- The genetic association of RUNX3 with ankylosing spondylitis can be explained by allele-specific effects on IRF4 recruitment that alter gene expression.Annals of the rheumatic diseases · 2016Article
- Quantitative Histone Mass Spectrometry Identifies Elevated Histone H3 Lysine 27 (Lys27) Trimethylation in Melanoma.Molecular & cellular proteomics : MCP · 2016Article
- The cnidarian origin of the proto-oncogenes NF-κB/STAT and WNT-like oncogenic pathway drives the ctenophores (Review).International journal of oncology · 2015Review
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Correlative and functional studies support the involvement of the RUNX gene family in haematological malignancies. To elucidate the role of epigenetics in RUNX inactivation, we evaluated promoter DNA methylation of RUNX1, 2, and 3 in 23 leukaemia cell lines and samples from acute myeloid leukaemia (AML), acute lymphocytic leukaemia (ALL) and myelodysplatic syndromes (MDS) patients. RUNX1 and RUNX2 gene promoters were mostly unmethylated in cell lines and clinical samples. Hypermethylation of RUNX3 was frequent among cell lines (74%) and highly variable among patient samples, with clear association to cytogenetic status. High frequency of RUNX3 hypermethylation (85% of the 20 studied cases) was found in AML patients with inv(16)(p13.1q22) compared to other AML subtypes (31% of the other 49 cases). RUNX3 hypermethylation was also frequent in ALL (100% of the six cases) but low in MDS (21%). In support of a functional role, hypermethylation of RUNX3 was correlated with low levels of protein, and treatment of cell lines with the DNA demethylating agent, decitabine, resulted in mRNA re-expression. Furthermore, relapse-free survival of non-inv(16)(p13.1q22) AML patients without RUNX3 methylation was significantly better (P = 0·016) than that of methylated cases. These results suggest that RUNX3 silencing is an important event in inv(16)(p13.1q22) leukaemias.
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