Osteoblast suppression in multiple myeloma bone disease

Juraj Adamik, Deborah L. Galson, G. David Roodman

Research output: Contribution to journalReview article

7 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)62-70
Number of pages9
JournalJournal of Bone Oncology
Volume13
DOIs
StatePublished - Nov 2018

Keywords

  • BMSCs
  • Bone microenvironment
  • Epigenetic
  • Genomic
  • Multiple myeloma bone disease
  • Osteoblast
  • Senescence

ASJC Scopus subject areas

  • Oncology

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