ArticleNature communications2015
Epigenomic evolution in diffuse large B-cell lymphomas.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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
85 citing papers in PubMed, 126 citations in OpenAlex.
- SWOG 1918: A phase II/III randomized study of R-miniCHOP with or without oral azacitidine (CC-486) in participants age 75 years or older with newly diagnosed aggressive non-Hodgkin lymphomas - Aiming to improve therapy, outcomes, and validate a prospective frailty tool.Journal of geriatric oncology · 2022Trial
- Discovery of Candidate DNA Methylation Cancer Driver Genes.Cancer discovery · 2021Trial
- Epigenetic priming with azacitidine-BEAM versus decitabine-BEAM conditioning for autologous transplantation in non-Hodgkin's lymphoma.Bone marrow transplantation · 2026Article
- Phase I study of oral azacitidine plus salvage chemotherapy in relapsed/refractory diffuse large B-cell lymphoma.Annals of hematology · 2026Article
- Human pancreatic progenitor organoids define genetic and epigenetic barriers to early PDAC transformation.Developmental cell · 2026Article
- Spatially decoding genotype-associated epigenetic landscapes in human lymphoma FFPE tissues via epi-Patho-DBiT.Nature communications · 2026Article
- Automatic Blood Protein Enrichment by Magnetic-COF Polymers.Analytical chemistry · 2026Article
- Local Promoter Methylation Disorder algorithm reveals bidirectional epigenetic disruption in DNMT3A-mutated AML and predicts azacitidine treatment response.Frontiers in oncology · 2026Article
- Unraveling the Epigenetic Landscape of Mature B Cell Neoplasia: Mechanisms, Biomarkers, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Methylation aberrations and genomic instability synergistically drive the evolution of intrahepatic cholangiocarcinoma.Epigenomics · 2025Article
- DNA Methylation Epitypes of Burkitt Lymphoma with Distinct Molecular and Clinical Features.Blood cancer discovery · 2025Article
- Increased local DNA methylation disorder in AMLs with DNMT3A-destabilizing variants and its clinical implication.Nature communications · 2025Article
- Azacitidine followed by R-GDP in transplant-ineligible relapsed/refractory diffuse large B-cell lymphoma: preliminary results from a multicenter, phase II study.Therapeutic advances in hematology · 2025Article
- A Mitochondria-Targeting SIRT3 Inhibitor with Activity against Diffuse Large B Cell Lymphoma.Journal of medicinal chemistry · 2024Article
- Epigenetics and environmental health.Frontiers of medicine · 2024Review
- Review
- Simulating Interclonal Interactions in Diffuse Large B-Cell Lymphoma.Bioengineering (Basel, Switzerland) · 2023Article
- Reuniting philosophy and science to advance cancer research.Biological reviews of the Cambridge Philosophical Society · 2023Article
- Metheor: Ultrafast DNA methylation heterogeneity calculation from bisulfite read alignments.PLoS computational biology · 2023Article
- Molecular characterization of Richter syndrome identifies de novo diffuse large B-cell lymphomas with poor prognosis.Nature communications · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of epigenomic alterations to tumour progression and relapse is not well characterized. Here we characterize an association between disease progression and DNA methylation in diffuse large B-cell lymphoma (DLBCL). By profiling genome-wide DNA methylation at single-base pair resolution in thirteen DLBCL diagnosis-relapse sample pairs, we show that DLBCL patients exhibit heterogeneous evolution of tumour methylomes during relapse. We identify differentially methylated regulatory elements and determine a relapse-associated methylation signature converging on key pathways such as transforming growth factor-β (TGF-β) receptor activity. We also observe decreased intra-tumour methylation heterogeneity from diagnosis to relapsed tumour samples. Relapse-free patients display lower intra-tumour methylation heterogeneity at diagnosis compared with relapsed patients in an independent validation cohort. Furthermore, intra-tumour methylation heterogeneity is predictive of time to relapse. Therefore, we propose that epigenomic heterogeneity may support or drive the relapse phenotype and can be used to predict DLBCL relapse.
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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.