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- W2890174450 endingPage "70" @default.
- W2890174450 startingPage "62" @default.
- W2890174450 abstract "Multiple myeloma (MM) is the most frequent cancer to involve the skeleton with patients developing osteolytic bone lesions due to hyperactivation of osteoclasts and suppression of BMSCs differentiation into functional osteoblasts. Although new therapies for MM have greatly improved survival, MM remains incurable for most patients. Despite the major advances in current anti-MM and anti-resorptive treatments that can significantly improve osteolytic bone lysis, many bone lesions can persist even after therapeutic remission of active disease. Bone marrow mesenchymal stem cells (BMSCs) from MM patients are phenotypically distinct from their healthy counterparts and the mechanisms associated with the long-term osteogenic suppression are largely unknown. In this review we will highlight recent results of transcriptomic profiling studies that provide new insights into the establishment and maintenance of the persistent pathological alterations in MM-BMSCs that occur in MM. We will we discuss the role of genomic instabilities and senescence in propagating the chronically suppressed state and pro-inflammatory phenotype associated with MM-BMSCs. Lastly we describe the role of epigenetic-based mechanisms in regulating osteogenic gene expression to establish and maintain the pro-longed suppression of MM-BMSC differentiation into functional OBs." @default.
- W2890174450 created "2018-09-27" @default.
- W2890174450 creator A5012356468 @default.
- W2890174450 creator A5018507303 @default.
- W2890174450 creator A5019561937 @default.
- W2890174450 date "2018-11-01" @default.
- W2890174450 modified "2023-10-06" @default.
- W2890174450 title "Osteoblast suppression in multiple myeloma bone disease" @default.
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- W2890174450 doi "https://doi.org/10.1016/j.jbo.2018.09.001" @default.
- W2890174450 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6303385" @default.