ArticleThe Journal of clinical investigation2013
Integrated genetic and epigenetic analysis of childhood acute lymphoblastic leukemia.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- HSC commitment-associated epigenetic signature is prognostic in acute myeloid leukemia.The Journal of clinical investigation · 2014Pooled it
- Specific molecular signatures predict decitabine response in chronic myelomonocytic leukemia.The Journal of clinical investigation · 2015Trial
- A therapeutic trial of decitabine and vorinostat in combination with chemotherapy for relapsed/refractory acute lymphoblastic leukemia.American journal of hematology · 2014Trial
- Comprehensive Epigenome-Wide Profiling Reveals Distinctive DNA Methylation Signatures and Potential Prognostic Biomarkers in Mexican Pediatric B-ALL.International journal of molecular sciences · 2025Article
- DNA methylation profiles and cancer in children conceived after assisted reproductive technology.Clinical epigenetics · 2025Article
- Rapid epigenomic classification of acute leukemia.Nature genetics · 2025Article
- Age-Driven Genetic and Epigenetic Heterogeneity in B-ALL.International journal of molecular sciences · 2025Review
- Histone-, Receptor-, and Integrin-Related Gene Products and ADAM28 as Relevant to B-Cell Acute Lymphoblastic Leukemia (B-ALL).Current issues in molecular biology · 2025Article
- Polyamines at the crossroad between cell metabolism and epigenetic regulation in acute leukemias.Cell death discovery · 2025Review
- KMT2A degradation is observed in decitabine-responsive acute lymphoblastic leukemia cells.Molecular oncology · 2025Article
- Integrated systems biology analysis of acute lymphoblastic leukemia: unveiling molecular signatures and drug repurposing opportunities.Annals of hematology · 2024Article
- Mitochondria and Acute Leukemia: A Clinician's Perspective.International journal of molecular sciences · 2024Review
- Unraveling Copy Number Alterations in Pediatric B-Cell Acute Lymphoblastic Leukemia: Correlation with Induction Phase Remission Using MLPA.Asian Pacific journal of cancer prevention : APJCP · 2024Observational
- Article
- The pros and cons of probiotic use in pediatric oncology patients following treatment for acute lymphoblastic leukemia.Frontiers in pediatrics · 2024Review
- Epigenomic mapping reveals distinct B cell acute lymphoblastic leukemia chromatin architectures and regulators.Cell genomics · 2023Article
- MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia.Nature communications · 2023Article
- Optical Genome Mapping Identifies Novel Recurrent Structural Alterations in ChildhoodHemaSphere · 2023Article
- TCF1/LEF1 triggers Wnt-dependent chemokine/cytokine-induced inflammation and cadherin pathways to drive T-ALL cell migration.Biochemistry and biophysics reports · 2023Article
- Effects of post-transplant maintenance therapy with decitabine prophylaxis on the relapse for acute lymphoblastic leukemia.Bone marrow transplantation · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Acute lymphoblastic leukemia (ALL) is the commonest childhood malignancy and is characterized by recurring structural genetic alterations. Previous studies of DNA methylation suggest epigenetic alterations may also be important, but an integrated genome-wide analysis of genetic and epigenetic alterations in ALL has not been performed. We analyzed 137 B-lineage and 30 T-lineage childhood ALL cases using microarray analysis of DNA copy number alterations and gene expression, and genome-wide cytosine methylation profiling using the HpaII tiny fragment enrichment by ligation-mediated PCR (HELP) assay. We found that the different genetic subtypes of ALL are characterized by distinct DNA methylation signatures that exhibit significant correlation with gene expression profiles. We also identified an epigenetic signature common to all cases, with correlation to gene expression in 65% of these genes, suggesting that a core set of epigenetically deregulated genes is central to the initiation or maintenance of lymphoid transformation. Finally, we identified aberrant methylation in multiple genes also targeted by recurring DNA copy number alterations in ALL, suggesting that these genes are inactivated far more frequently than suggested by structural genomic analyses alone. Together, these results demonstrate subtype- and disease-specific alterations in cytosine methylation in ALL that influence transcriptional activity, and are likely to exert a key role in leukemogenesis.
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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.