ArticleMediators of inflammation2011
Angiogenesis-related cytokines, RANKL, and osteoprotegerin in multiple myeloma patients in relation to clinical features and response to treatment.
Article in Mediators of inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- The Clinical Relevance of Selected Cytokines in Newly Diagnosed Multiple Myeloma Patients.Biomedicines · 2023Article
- The RANK-RANKL-OPG System: A Multifaceted Regulator of Homeostasis, Immunity, and Cancer.Medicina (Kaunas, Lithuania) · 2023Review
- Anti-Angiogenic Activity of Drugs in Multiple Myeloma.Cancers · 2023Review
- The HGF/Met/NF-κB Pathway Regulates RANKL Expression in Osteoblasts and Bone Marrow Stromal Cells.International journal of molecular sciences · 2020Article
- Possible Prognostic Potential of RANKL and OPG in Metastatic Breast Cancer Egyptian Females.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Harnessing the versatile role of OPG in bone oncology: counterbalancing RANKL and TRAIL signaling and beyond.Clinical & experimental metastasis · 2020Review
- Erythropoietin treatment in murine multiple myeloma: immune gain and bone loss.Scientific reports · 2016Article
- Article
- Nuclear factor-kappa B ligand and osteoprotegerin levels in serum and gingival crevicular fluid in patients with bone metastases treated with zoledronic acid.Medical oncology (Northwood, London, England) · 2014Article
- Angiogenesis and its therapeutic opportunities.Mediators of inflammation · 2013Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An essential cytokine system for the osteoclast biology in multiple myeloma (MM) consists of the receptor of activator of NF-κB ligand (RANKL), its receptor (RANK), and the soluble decoy receptor, osteoprotegerin (OPG). Myeloma cells cause imbalance in OPG/RANKL interactions. We measured serum levels of OPG, soluble (s) RANKL, sRANKL/OPG ratio, markers of disease activity [LDH, CRP, interleukin-6 (IL-6), β2-microglobulin (B2M)], and angiogenic factors [hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF)], in 54 newly diagnosed MM patients and in 25 of them in plateau phase. All the above values were higher in MM patients compared to controls and decreased in plateau phase. sRANKL and RANKL/OPG were higher with advancing disease stage and skeletal grade. Significant correlations were found among RANKL and RANKL/OPG with HGF, LDH, VEGF, IL-6, and B2M. In conclusion, RANKL and OPG play significant roles in MM pathophysiology, as regulators of bone turnover and mediators of angiogenesis.
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