ArticleScientific reports2019
Multiple myeloma increases nerve growth factor and other pain-related markers through interactions with the bone microenvironment.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Concordant Shared Transcriptomic Signatures and Candidate Regulatory Features in Chronic Lymphocytic Leukemia and Multiple Myeloma.Oncology research · 2026Article
- Not Just Neurons: Pain Is Orchestrated in Partnership with Many Non-neuronal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Unraveling Obesity and Multiple Myeloma: Insights from Epidemiology and Molecular Mechanisms.Current obesity reports · 2025Review
- Metastatic Infiltration of Nervous Tissue and Periosteal Nerve Sprouting in Multiple Myeloma-Induced Bone Pain in Mice and Human.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Obesity as a risk factor for multiple myeloma: insight on the role of adipokines.Pathology oncology research : POR · 2023Review
- Obesity and myeloma: Clinical and mechanistic contributions to disease progression.Frontiers in endocrinology · 2023Review
- Transplantation of autologous bone marrow pre-loadedOncotarget · 2022Article
- JZL184, A Monoacylglycerol Lipase Inhibitor, Induces Bone Loss in a Multiple Myeloma Model of Immunocompetent Mice.Calcified tissue international · 2020Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Interactions between multiple myeloma (MM) and bone marrow (BM) are well documented to support tumour growth, yet the cellular mechanisms underlying pain in MM are poorly understood. We have used in vivo murine models of MM to show significant induction of nerve growth factor (NGF) by the tumour-bearing bone microenvironment, alongside other known pain-related characteristics such as spinal glial cell activation and reduced locomotion. NGF was not expressed by MM cells, yet bone stromal cells such as osteoblasts expressed and upregulated NGF when cultured with MM cells, or MM-related factors such as TNF-α. Adiponectin is a known MM-suppressive BM-derived factor, and we show that TNF-α-mediated NGF induction is suppressed by adiponectin-directed therapeutics such as AdipoRON and L-4F, as well as NF-κB signalling inhibitor BMS-345541. Our study reveals a further mechanism by which cellular interactions within the tumour-bone microenvironment contribute to disease, by promoting pain-related properties, and suggests a novel direction for analgesic development.
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Registered trials
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