ArticleClinical epigenetics2023
DNA methylation landscape reveals LIN7A as a decitabine-responsive marker in patients with t(8;21) acute myeloid leukemia.
Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Efficacy and safety of FDA-approved IDH inhibitors in the treatment of IDH mutated acute myeloid leukemia: a systematic review and meta-analysis.Clinical epigenetics · 2023Pooled it
- Spatial Transcriptomics Unveils the Blueprint of Mammalian Lung Development.Genomics, proteomics & bioinformatics · 2026Article
- miR-182 promoter hypermethylation predicts the better outcome of AML patients treated with AZA + VEN in a real-world setting.Clinical epigenetics · 2025Article
- The Proteasome-Family-Members-Based Prognostic Model Improves the Risk Classification for Adult Acute Myeloid Leukemia.Biomedicines · 2024Article
- Fetal hemoglobin induction in azacytidine responders enlightens methylation patterns related to blast clearance in higher-risk MDS and CMML.Clinical epigenetics · 2024Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite its inconsistent response rate, decitabine, a demethylating agent, is often used as a non-intensive alternative therapeutic agent for acute myeloid leukemia (AML). It has been reported that relapsed/refractory AML patients with t(8;21) translocation achieved better clinical outcomes with a decitabine-based combination regimen than other AML subtypes; however, the mechanisms underlying this phenomenon remain unknown. Herein, the DNA methylation landscape of de novo patients with the t(8;21) translocation was compared with that of patients without the translocation. Moreover, the methylation changes induced by decitabine-based combination regimens in de novo/complete remission paired samples were investigated to elucidate the mechanisms underlying the better responses observed in t(8;21) AML patients treated with decitabine.
methodsThirty-three bone marrow samples from 28 non-M3 AML patients were subjected to DNA methylation sequencing to identify the differentially methylated regions and genes of interest. TCGA-AML Genome Atlas-AML transcriptome dataset was used to identify decitabine-sensitive genes that were downregulated following exposure to a decitabine-based regimen. In addition, the effect of decitabine-sensitive gene on cell apoptosis was examined in vitro using Kasumi-1 and SKNO-1 cells.
resultsA total of 1377 differentially methylated regions that specifically responsive to decitabine in t(8;21) AML were identified, of which 210 showed hypomethylation patterns following decitabine treatment aligned with the promoter regions of 72 genes. And the methylation-silencing genes, LIN7A, CEBPA, BASP1, and EMB were identified as critical decitabine-sensitive genes in t(8;21) AML. Moreover, AML patients with hypermethylated LIN7A and reduced LIN7A expression had poor clinical outcomes. Meanwhile, the downregulation of LIN7A inhibited decitabine/cytarabine combination treatment-induced apoptosis in t(8;21) AML cells in vitro.
conclusionThe findings of this study suggest that LIN7A is a decitabine-sensitive gene in t(8;21) AML patients that may serve as a prognostic biomarker for decitabine-based therapy.
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