ArticleLeukemia2014
Promiscuous MYC locus rearrangements hijack enhancers but mostly super-enhancers to dysregulate MYC expression in multiple myeloma.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.
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Who cites it
177 citing papers in PubMed, 264 citations in OpenAlex.
- Concomitant gain of 1q21 and MYC translocation define a poor prognostic subgroup of hyperdiploid multiple myeloma.Haematologica · 2016Trial
- GP130 activation induces myeloma and collaborates with MYC.The Journal of clinical investigation · 2014Trial
- Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.Cancer research · 2026Article
- Cancer-associated fusion transcripts: mechanisms, functional roles, and clinical implications.Clinical and experimental medicine · 2026Review
- Genetic architecture of multiple myeloma: From somatic alterations to germline susceptibility and clinical implications.Translational oncology · 2026Review
- From fragments to full pictures: how long-read sequencing platforms are revolutionizing oncology research.Molecular biology reports · 2026Review
- The Histone Modifier KANSL2 Is an Actionable Biomarker in Multiple Myeloma.Molecular cancer therapeutics · 2026Article
- A High-Fiber, Plant-Based Diet in Myeloma Precursor Disorders: Results from the NUTRIVENTION Clinical Trial and Preclinical Vk*MYC Model.Cancer discovery · 2026Article
- Crosstalk BetweenCancers · 2026Review
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- An odyssey of monoclonal gammopathies: focusing on precursors and the progression from MGUS and SMM to multiple Myeloma, with a brief overview of novel therapeutic strategies.Clinical and experimental medicine · 2026Review
- Synergistic targeting of the ARID2-MYC axis by pomalidomide and panobinostat overcomes intrinsic IMiD resistance in multiple myeloma.Scientific reports · 2026Article
- Super-enhancers mediates SLC7A11 via FOXA1 to regulate disulfidptosis in prostate cancer.Cell death & disease · 2025Article
- Microbiome modulation uncouples efficacy and toxicity induced by immune checkpoint blockade in mouse multiple myeloma.Nature communications · 2025Article
- Guidelines for the testing and reporting of cytogenetic results for risk stratification of multiple myeloma: a report of the Cancer Genomics Consortium Plasma Cell Neoplasm Working Group.Blood cancer journal · 2025Review
- Immunocompetent mouse models of multiple myeloma.Seminars in hematology · 2025Review
- Super-enhancers in immune system regulation: mechanisms, pathological reprogramming, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Super enhancers as key drivers of gene regulatory networks in normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2025Review
- Transcriptional regulation by MYC: an emerging new model.Oncogene · 2025Review
- Selective Enhancer Gain-of-Function Deregulates MYC Expression in Multiple Myeloma.Cancer research · 2024Article
117 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
MYC locus rearrangements-often complex combinations of translocations, insertions, deletions and inversions-in multiple myeloma (MM) were thought to be a late progression event, which often did not involve immunoglobulin genes. Yet, germinal center activation of MYC expression has been reported to cause progression to MM in an MGUS (monoclonal gammopathy of undetermined significance)-prone mouse strain. Although previously detected in 16% of MM, we find MYC rearrangements in nearly 50% of MM, including smoldering MM, and they are heterogeneous in some cases. Rearrangements reposition MYC near a limited number of genes associated with conventional enhancers, but mostly with super-enhancers (e.g., IGH, IGL, IGK, NSMCE2, TXNDC5, FAM46C, FOXO3, IGJ, PRDM1). MYC rearrangements are associated with a significant increase of MYC expression that is monoallelic, but MM tumors lacking a rearrangement have biallelic MYC expression at significantly higher levels than in MGUS. We also have shown that germinal center activation of MYC does not cause MM in a mouse strain that rarely develops spontaneous MGUS. It appears that increased MYC expression at the MGUS/MM transition usually is biallelic, but sometimes can be monoallelic if there is an MYC rearrangement. Our data suggest that MYC rearrangements, regardless of when they occur during MM pathogenesis, provide one event that contributes to tumor autonomy.
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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.