A bone paradigm challenging the standard model of myeloma oncogenesis.
Bone inflamm'aging
Bone marrow microenvironment
Endosteal niche
Gaucher disease
Mesenchymal-stromal to osteoblast transition (MS-to-ObT)
Monoclonal gammopathy of undetermined significance
Multiple myeloma
Tissue disruption-induced cellular stochasticity (TiDiS)
Journal
Critical reviews in oncology/hematology
ISSN: 1879-0461
Titre abrégé: Crit Rev Oncol Hematol
Pays: Netherlands
ID NLM: 8916049
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
15
03
2021
revised:
02
02
2022
accepted:
16
02
2022
pubmed:
21
2
2022
medline:
6
4
2022
entrez:
20
2
2022
Statut:
ppublish
Résumé
The standard model of multiple myeloma (MM) oncogenesis from monoclonal gammopathy of undetermined significance (MGUS) relies on genetic instability in the normal counterparts of MM cells. However, the importance of both MGUS-associated and MM-induced bone changes has been recently re-appraised, emphasizing the bone microenvironment (BME) as a tissue of significance. In this review, we propose that early BME alterations (bone senescence and inflammation, i.e., bone inflamm'aging) at the pre-MGUS stage could be causal, and not simply permissive, and creative of phenotypic instability and genetic alterations thanks to the concept of tissue disruption-induced cell stochasticity (TiDiS). This article offers a bone scenario challenging the chromosome-and-gene-centric standard model of MM oncogenesis. The high incidence of both MGUS and MM in Gaucher disease supports such a scenario.
Identifiants
pubmed: 35183697
pii: S1040-8428(22)00064-6
doi: 10.1016/j.critrevonc.2022.103640
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
103640Informations de copyright
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