ArticleProceedings of the National Academy of Sciences of the United States of America2009
Epigenetic changes during disease progression in a murine model of human chronic lymphocytic leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 85 citations in OpenAlex.
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- P66Shc: A Pleiotropic Regulator of B Cell Trafficking and a Gatekeeper in Chronic Lymphocytic Leukemia.Cancers · 2020Review
- p66Shc deficiency in the Eμ-TCL1 mouse model of chronic lymphocytic leukemia enhances leukemogenesis by altering the chemokine receptor landscape.Haematologica · 2019Article
- Linking aberrant chromatin features in chronic lymphocytic leukemia to transcription factor networks.Molecular systems biology · 2019Article
- BRD4 interacts with PML/RARα in acute promyelocytic leukemia.Frontiers of medicine · 2018Article
- Novel role of prostate apoptosis response-4 tumor suppressor in B-cell chronic lymphocytic leukemia.Blood · 2018Article
- Proteomics and metabolomics identify molecular mechanisms of aging potentially predisposing for chronic lymphocytic leukemia.Molecular & cellular proteomics : MCP · 2018Article
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- Alterations in DNA methylation/demethylation intermediates predict clinical outcome in chronic lymphocytic leukemia.Oncotarget · 2017Article
- NF-κB p50 (Blood · 2017Article
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- Hsp90 inhibition increases SOCS3 transcript and regulates migration and cell death in chronic lymphocytic leukemia.Oncotarget · 2016Article
- TCL1 transgenic mouse model as a tool for the study of therapeutic targets and microenvironment in human B-cell chronic lymphocytic leukemia.Cell death & disease · 2016Review
- Analysis of the miRNA-mRNA-lncRNA networks in ER+ and ER- breast cancer cell lines.Journal of cellular and molecular medicine · 2015Article
- Master redox regulator Trx1 upregulates SMYD1 & modulates lysine methylation.Biochimica et biophysica acta · 2015Article
- T-cell number and subtype influence the disease course of primary chronic lymphocytic leukaemia xenografts in alymphoid mice.Disease models & mechanisms · 2015Article
- Review
- Genetic and epigenetic profiling of CLL disease progression reveals limited somatic evolution and suggests a relationship to memory-cell development.Blood cancer journal · 2015Article
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Authors and funding
21 authors at 8 institutions in 3 countries.
Funding
Abstract
Epigenetic alterations, including gain or loss of DNA methylation, are a hallmark of nearly every malignancy. Changes in DNA methylation can impact expression of cancer-related genes including apoptosis regulators and tumor suppressors. Because such epigenetic changes are reversible, they are being aggressively investigated as potential therapeutic targets. Here we use the Emu-TCL1 transgenic mouse model of chronic lymphocytic leukemia (CLL) to determine the timing and patterns of aberrant DNA methylation, and to investigate the mechanisms that lead to aberrant DNA methylation. We show that CLL cells from Emu-TCL1 mice at various stages recapitulate epigenetic alterations seen in human CLL. Aberrant methylation of promoter sequences is observed as early as 3 months of age in these animals, well before disease onset. Abnormally methylated promoter regions include binding sites for the transcription factor FOXD3. We show that loss of Foxd3 expression due to an NF-kappaB p50/p50:HDAC1 repressor complex occurs in TCL1-positive B cells before methylation. Therefore, specific transcriptional repression is an early event leading to epigenetic silencing of target genes in murine and human CLL. These results provide strong rationale for the development of strategies to target NF-kappaB components in CLL and potentially other B-cell malignancies.
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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.