Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory.
MGUS
bone lesion
bone marrow microenvironment
cell-to-cell heterogeneity
endosteal niche
gene expression noise
multiple myeloma
oncogenesis
plasma cells
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
04 Aug 2020
04 Aug 2020
Historique:
received:
26
06
2020
revised:
31
07
2020
accepted:
02
08
2020
entrez:
8
8
2020
pubmed:
8
8
2020
medline:
8
8
2020
Statut:
epublish
Résumé
The standard model of multiple myeloma (MM) relies on genetic instability in the normal counterparts of MM cells. MM-induced lytic bone lesions are considered as end organ damages. However, bone is a tissue of significance in MM and bone changes could be at the origin/facilitate the emergence of MM. We propose the tissue disruption-induced cell stochasticity (TiDiS) theory for MM oncogenesis that integrates disruption of the microenvironment, differentiation, and genetic alterations. It starts with the observation that the bone marrow endosteal niche controls differentiation. As decrease in cellular stochasticity occurs thanks to cellular interactions in differentiating cells, the initiating role of bone disruption would be in the increase of cellular stochasticity. Thus, in the context of polyclonal activation of B cells, memory B cells and plasmablasts would compete for localizing in endosteal niches with the risk that some cells cannot fully differentiate if they cannot reside in the niche because of a disrupted microenvironment. Therefore, they would remain in an unstable state with residual proliferation, with the risk that subclones may transform into malignant cells. Finally, diagnostic and therapeutic perspectives are provided.
Identifiants
pubmed: 32759688
pii: cancers12082158
doi: 10.3390/cancers12082158
pmc: PMC7463431
pii:
doi:
Types de publication
Journal Article
Langues
eng
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