ArticleCancer research2009
Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- A Japanese family of hereditary diffuse gastric cancer with a germline pathogenic variant of CTNN1A detected via comprehensive genome profiling.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- The Role of CTNNA1 in Malignancies: An Updated Review.Journal of Cancer · 2023Review
- Targeting β-catenin in acute myeloid leukaemia: past, present, and future perspectives.Bioscience reports · 2022Review
- Age-related inflammatory bone marrow microenvironment induces ineffective erythropoiesis mimicking del(5q) MDS.Leukemia · 2018Article
- Recurrent genetic defects on chromosome 5q in myeloid neoplasms.Oncotarget · 2017Article
- CTNNA1 hypermethylation, a frequent event in acute myeloid leukemia, is independently associated with an adverse outcome.Oncotarget · 2016Article
- Lipopolysaccharide-induced α-catenin downregulation enhances the motility of human colorectal cancer cells in an NF-κB signaling-dependent manner.OncoTargets and therapy · 2016Article
- Clinical implications of the quantitative detection of ID4 gene methylation in myelodysplastic syndrome.European journal of medical research · 2015Article
- Epigenetics of myelodysplastic syndromes.Leukemia · 2014Review
- Poly(ADP-ribose) polymerase inhibitor CEP-8983 synergizes with bendamustine in chronic lymphocytic leukemia cells in vitro.Leukemia research · 2014Article
- Submicroscopic deletion of 5q involving tumor suppressor genes (CTNNA1, HSPA9) and copy neutral loss of heterozygosity associated with TET2 and EZH2 mutations in a case of MDS with normal chromosome and FISH results.Molecular cytogenetics · 2014Article
- α-catenin. A tumor suppressor beyond adherens junctions.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- Pretransplantation therapy with azacitidine vs induction chemotherapy and posttransplantation outcome in patients with MDS.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2012Article
- Topography, clinical, and genomic correlates of 5q myeloid malignancies revisited.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012Article
- Allelic methylation levels of the noncoding VTRNA2-1 located on chromosome 5q31.1 predict outcome in AML.Blood · 2012Article
- Histone methylation in myelodysplastic syndromes.Epigenomics · 2011Review
- Unraveling the molecular pathophysiology of myelodysplastic syndromes.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011Review
- Knockdown of Hspa9, a del(5q31.2) gene, results in a decrease in hematopoietic progenitors in mice.Blood · 2011Article
- Silence of HIN-1 expression through methylation of its gene promoter in gastric cancer.World journal of gastroenterology · 2011Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML). The putative gene(s) deleted and responsible for the pathogenesis of these poor prognosis hematologic disorders remain controversial. This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS. In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed. In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but not in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to AML. CTNNA1 expression was lowest in AML/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation. Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed AML cell lines and primary leukemias, with the most repressive state correlating with DNA methylation. These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component of leukemia progression in patients with both 5q- and non-5q- myeloid malignancies.
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