ArticlePloS one2015
Whole Genome Sequence of Multiple Myeloma-Prone C57BL/KaLwRij Mouse Strain Suggests the Origin of Disease Involves Multiple Cell Types.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Modeling bone marrow microenvironment and hematopoietic dysregulation in Gaucher disease through VavCre mediated Gba deletion.Human molecular genetics · 2025Article
- Immunocompetent mouse models of multiple myeloma.Seminars in hematology · 2025Review
- Combination adjuvant improves influenza virus immunity by downregulation of immune homeostasis genes in lymphocytes.ImmunoHorizons · 2025Article
- Deciphering the genetics and mechanisms of predisposition to multiple myeloma.Nature communications · 2024Article
- Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024Review
- Targeting the ribosome to treat multiple myeloma.Molecular therapy. Oncology · 2024Article
- Article
- Obesity and myeloma: Clinical and mechanistic contributions to disease progression.Frontiers in endocrinology · 2023Review
- Longitudinal single-cell analysis of a myeloma mouse model identifies subclonal molecular programs associated with progression.Nature communications · 2021Article
- Orthogonal targeting of osteoclasts and myeloma cells for radionuclide stimulated dynamic therapy induces multidimensional cell death pathways.Theranostics · 2021Article
- Laboratory Mice - A Driving Force in Immunopathology and Immunotherapy Studies of Human Multiple Myeloma.Frontiers in immunology · 2021Review
- Characterization of the role of Samsn1 loss in multiple myeloma development.FASEB bioAdvances · 2020Article
- Chronic intermittent hypoxia enhances disease progression in myeloma-resistant mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- Prevention Is the Best Treatment: The Case for Understanding the Transition from Monoclonal Gammopathy of Undetermined Significance to Myeloma.International journal of molecular sciences · 2018Review
- Osteoblast suppression in multiple myeloma bone disease.Journal of bone oncology · 2018Review
- The genetic landscape of 5T models for multiple myeloma.Scientific reports · 2018Article
- Extracellular matrix and the myeloid-in-myeloma compartment: balancing tolerogenic and immunogenic inflammation in the myeloma niche.Journal of leukocyte biology · 2017Review
- The Evolution and Expression Pattern of Human Overlapping lncRNA and Protein-coding Gene Pairs.Scientific reports · 2017Article
- Angioimmunoblastic T cell lymphoma: novel molecular insights by mutation profiling.Oncotarget · 2017Article
- Challenges and Promises of Genetic Stratification of Risk in Multiple Myeloma.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2017Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Monoclonal gammopathy of undetermined significance (MGUS) is the requisite precursor to multiple myeloma (MM), a malignancy of antibody-producing plasma B-cells. The genetic basis of MGUS and its progression to MM remains poorly understood. C57BL/KaLwRij (KaLwRij) is a spontaneously-derived inbred mouse strain with a high frequency of benign idiopathic paraproteinemia (BIP), a phenotype with similarities to MGUS including progression to MM. Using mouse haplotype analysis, human MM SNP array data, and whole exome and whole genome sequencing of KaLwRij mice, we identified novel KaLwRij gene variants, including deletion of Samsn1 and deleterious point mutations in Tnfrsf22 and Tnfrsf23. These variants significantly affected multiple cell types implicated in MM pathogenesis including B-cells, macrophages, and bone marrow stromal cells. These data demonstrate that multiple cell types contribute to MM development prior to the acquisition of somatic driver mutations in KaLwRij mice, and suggest that MM may an inherently non-cell autonomous malignancy.
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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.