ArticleBlood2021
Expression of NrasQ61R and MYC transgene in germinal center B cells induces a highly malignant multiple myeloma in mice.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- SSTNSignal transduction and targeted therapy · 2026Article
- Gene mutation in metabolism syndrome with hematologic tumor: A retrospective cohort study.Clinical and experimental medicine · 2026Observational
- Inhibition of FOXM1 Synergizes with BH3 Mimetics Venetoclax and Sonrotoclax in Killing Multiple Myeloma Cells through Repressing MYC Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Immunocompetent mouse models of multiple myeloma.Seminars in hematology · 2025Review
- Orphan nuclear receptor NR2E3 is a new molecular vulnerability in solid tumors by activating p53.Cell death & disease · 2025Article
- Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024Review
- Mechanisms of the role of proto-oncogene activation in promoting malignant transformation of mature B cells.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Research Progress on Pyroptosis in Hematological Malignancies.Current treatment options in oncology · 2023Review
- Drug combinations identified by high-throughput screening promote cell cycle transition and upregulate Smad pathways in myeloma.Cancer letters · 2023Article
- Molecular characterization stratifies VQ myeloma cells into two clusters with distinct risk signatures and drug responses.Oncogene · 2023Article
- Mouse models of human multiple myeloma subgroups.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Preclinical models for prediction of immunotherapy outcomes and immune evasion mechanisms in genetically heterogeneous multiple myeloma.Nature medicine · 2023Article
- Malignant clonal evolution drives multiple myeloma cellular ecological diversity and microenvironment reprogramming.Molecular cancer · 2022Article
- Stromal remodeling regulates dendritic cell abundance and activity in the tumor microenvironment.Cell reports · 2022Article
- Ponatinib sensitizes myeloma cells to MEK inhibition in the high-risk VQ model.Scientific reports · 2022Article
- [Establishment and comparison of three human multiple myeloma cell line transplantation models in mice].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022Article
- KRAS and RAS-MAPK Pathway Deregulation in Mature B Cell Lymphoproliferative Disorders.Cancers · 2022Review
- Review
- Review
- Laboratory Mice - A Driving Force in Immunopathology and Immunotherapy Studies of Human Multiple Myeloma.Frontiers in immunology · 2021Review
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25 authors at 6 institutions in 1 country.
Funding
Abstract
NRAS Q61 mutations are prevalent in advanced/relapsed multiple myeloma (MM) and correlate with poor patient outcomes. Thus, we generated a novel MM model by conditionally activating expression of endogenous NrasQ61R and an MYC transgene in germinal center (GC) B cells (VQ mice). VQ mice developed a highly malignant MM characterized by a high proliferation index, hyperactivation of extracellular signal-regulated kinase and AKT signaling, impaired hematopoiesis, widespread extramedullary disease, bone lesions, kidney abnormalities, preserved programmed cell death protein 1 and T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibition motif domain immune-checkpoint pathways, and expression of human high-risk MM gene signatures. VQ MM mice recapitulate most of the biological and clinical features of human advanced/high-risk MM. These MM phenotypes are serially transplantable in syngeneic recipients. Two MM cell lines were also derived to facilitate future genetic manipulations. Combination therapies based on MEK inhibition significantly prolonged the survival of VQ mice with advanced-stage MM. Our study provides a strong rationale to develop MEK inhibition-based therapies for treating advanced/relapsed MM.
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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.