ArticleProceedings of the National Academy of Sciences of the United States of America2023
Mouse models of human multiple myeloma subgroups.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Strong constitutive NF-κB signaling in B cells drives SLL/CLL-like lymphomagenesis and overcomes microenvironmental dependencies.Leukemia · 2026Article
- Human preclinical multiple myeloma in vitro models for disease modeling and therapy screening.Journal of biological engineering · 2025Review
- Modeling the Bone Marrow Niche in Multiple Myeloma: From 2D Cultures to 3D Systems.International journal of molecular sciences · 2025Review
- Immunocompetent mouse models of multiple myeloma.Seminars in hematology · 2025Review
- Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors.International journal of molecular sciences · 2024Article
- LILRB4 on multiple myeloma cells promotes bone lesion by p-SHP2/NF-κB/RELT signal pathway.Journal of experimental & clinical cancer research : CR · 2024Article
- The genomic landscape of Vk*MYC myeloma highlights shared pathways of transformation between mice and humans.Nature communications · 2024Article
- Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 3 countries.
Funding
Abstract
Multiple myeloma (MM), a tumor of germinal center (GC)-experienced plasma cells, comprises distinct genetic subgroups, such as the t(11;14)/CCND1 and the t(4;14)/MMSET subtype. We have generated genetically defined, subgroup-specific MM models by the GC B cell-specific coactivation of mouse Ccnd1 or MMSET with a constitutively active Ikk2 mutant, mimicking the secondary NF-κB activation frequently seen in human MM. Ccnd1/Ikk2ca and MMSET/Ikk2ca mice developed a pronounced, clonally restricted plasma cell outgrowth with age, accompanied by serum M spikes, bone marrow insufficiency, and bone lesions. The transgenic plasma cells could be propagated in vivo and showed distinct transcriptional profiles, resembling their human MM counterparts. Thus, we show that targeting the expression of genes involved in MM subgroup-specific chromosomal translocations into mouse GC B cells translates into distinct MM-like diseases that recapitulate key features of the human tumors, opening the way to a better understanding of the pathogenesis and therapeutic vulnerabilities of different MM subgroups.
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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.