ArticleThe EMBO journal2012
A novel molecular mechanism involved in multiple myeloma development revealed by targeting MafB to haematopoietic progenitors.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- MAFB: a key regulator of myeloid commitment involved in hematological diseases.Cell death discovery · 2025Review
- Mouse models of human multiple myeloma subgroups.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- β adrenergic signaling regulates hematopoietic stem and progenitor cell commitment and therapy sensitivity in multiple myeloma.Haematologica · 2022Article
- The DNA methylation landscape of multiple myeloma shows extensive inter- and intrapatient heterogeneity that fuels transcriptomic variability.Genome medicine · 2021Article
- Review
- Laboratory Mice - A Driving Force in Immunopathology and Immunotherapy Studies of Human Multiple Myeloma.Frontiers in immunology · 2021Review
- Pathogenesis of chronic lymphocytic leukemia and the development of novel therapeutic strategies.Journal of clinical and experimental hematopathology : JCEH · 2020Review
- Pathophysiology of chronic lymphocytic leukemia and human B1 cell development.International journal of hematology · 2020Review
- The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival.The Journal of biological chemistry · 2020Article
- RECQL4, Negatively Regulated by miR-10a-5p, Facilitates Cell Proliferation and Invasion via MAFB in Ovarian Cancer.Frontiers in oncology · 2020Article
- Are Leukaemic Stem Cells Restricted to a Single Cell Lineage?International journal of molecular sciences · 2019Review
- Regulatory mechanisms of B cell responses and the implication in B cell-related diseases.Journal of biomedical science · 2019Review
- Article
- Epigenetic Priming in Childhood Acute Lymphoblastic Leukemia.Frontiers in cell and developmental biology · 2019Review
- A multiple myeloma classification system that associates normal B-cell subset phenotypes with prognosis.Blood advances · 2018Article
- Lmo2 expression defines tumor cell identity during T-cell leukemogenesis.The EMBO journal · 2018Article
- MAFb protein confers intrinsic resistance to proteasome inhibitors in multiple myeloma.BMC cancer · 2018Article
- The Making of Leukemia.International journal of molecular sciences · 2018Review
- T-cell leukemogenesis is an inappropriate lineage decision-making process: implications for precision oncology.Molecular & cellular oncology · 2018Article
- Lineage choice decisions in B-cell development and leukemia.Stem cell investigation · 2018Article
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 2 countries.
Funding
Abstract
Understanding the cellular origin of cancer can help to improve disease prevention and therapeutics. Human plasma cell neoplasias are thought to develop from either differentiated B cells or plasma cells. However, when the expression of Maf oncogenes (associated to human plasma cell neoplasias) is targeted to mouse B cells, the resulting animals fail to reproduce the human disease. Here, to explore early cellular changes that might take place in the development of plasma cell neoplasias, we engineered transgenic mice to express MafB in haematopoietic stem/progenitor cells (HS/PCs). Unexpectedly, we show that plasma cell neoplasias arise in the MafB-transgenic mice. Beyond their clinical resemblance to human disease, these neoplasias highly express genes that are known to be upregulated in human multiple myeloma. Moreover, gene expression profiling revealed that MafB-expressing HS/PCs were more similar to B cells and tumour plasma cells than to any other subset, including wild-type HS/PCs. Consistent with this, genome-scale DNA methylation profiling revealed that MafB imposes an epigenetic program in HS/PCs, and that this program is preserved in mature B cells of MafB-transgenic mice, demonstrating a novel molecular mechanism involved in tumour initiation. Our findings suggest that, mechanistically, the haematopoietic progenitor population can be the target for transformation in MafB-associated plasma cell neoplasias.
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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.