ArticleLeukemia2016
Genomic disruption of the histone methyltransferase SETD2 in chronic lymphocytic leukaemia.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 81 citations in OpenAlex.
- Circulating tumor DNA predicts efficacy of a dual AKT/p70S6K inhibitor (LY2780301) plus paclitaxel in metastatic breast cancer: plasma analysis of the TAKTIC phase IB/II study.Molecular oncology · 2022Trial
- Genomic and transcriptomic correlates of Richter transformation in chronic lymphocytic leukemia.Blood · 2021Trial
- Trial
- Genetic polymorphisms of histone methyltransferase SETD2 predicts prognosis and chemotherapy response in Chinese acute myeloid leukemia patients.Journal of translational medicine · 2019Trial
- Leveraging a spectrum of cytogenomics methods for profiling complex karyotypes in chronic lymphocytic leukemia.Human genomics · 2026Article
- Article
- Aberrant Kupffer-like differentiation of hematopoietic stem cell is critical for the MDS pathogenesis in Setd2-deficient mice.Cell death and differentiation · 2026Article
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- Unraveling the Epigenetic Landscape of Mature B Cell Neoplasia: Mechanisms, Biomarkers, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Molecular Mechanisms in the Transformation from Indolent to Aggressive B Cell Malignancies.Cancers · 2025Review
- Chromoanagenesis Detection in Chronic Lymphocytic Leukemia.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Testicular large B-cell lymphoma is genetically similar to PCNSL and distinct from nodal DLBCL.HemaSphere · 2024Article
- Multiple omics levels of chronic lymphocytic leukemia.Cell death discovery · 2024Review
- Prognostic and therapeutic roles ofAging · 2024Article
- Advances in epigenetic alterations of chronic lymphocytic leukemia: from pathogenesis to treatment.Clinical and experimental medicine · 2024Review
- Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- Genomic Stratification of Hematological Malignancies.HemaSphere · 2023Article
- Clinical and genetic features of luscan-lumish syndrome associated with a novel de novo variant ofFrontiers in genetics · 2023Article
- Precision diagnostics in chronic lymphocytic leukemia: Past, present and future.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
38 authors at 14 institutions in 6 countries.
Funding
Abstract
Histone methyltransferases (HMTs) are important epigenetic regulators of gene transcription and are disrupted at the genomic level in a spectrum of human tumours including haematological malignancies. Using high-resolution single nucleotide polymorphism (SNP) arrays, we identified recurrent deletions of the SETD2 locus in 3% (8/261) of chronic lymphocytic leukaemia (CLL) patients. Further validation in two independent cohorts showed that SETD2 deletions were associated with loss of TP53, genomic complexity and chromothripsis. With next-generation sequencing we detected mutations of SETD2 in an additional 3.8% of patients (23/602). In most cases, SETD2 deletions or mutations were often observed as a clonal event and always as a mono-allelic lesion, leading to reduced mRNA expression in SETD2-disrupted cases. Patients with SETD2 abnormalities and wild-type TP53 and ATM from five clinical trials employing chemotherapy or chemo-immunotherapy had reduced progression-free and overall survival compared with cases wild type for all three genes. Consistent with its postulated role as a tumour suppressor, our data highlight SETD2 aberration as a recurrent, early loss-of-function event in CLL pathobiology linked to aggressive disease.
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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.