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Multiple Myeloma Associated Bone Disease
 
 
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Perspective

Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory

by
Jean-Pascal Capp
1,* and
Régis Bataille
2
1
Toulouse Biotechnology Institute, University of Toulouse, INSA, CNRS, INRAE, 31077 Toulouse, France
2
Faculty of Medicine, University of Angers, 49045 Angers, France
*
Author to whom correspondence should be addressed.
Cancers 2020, 12(8), 2158; https://doi.org/10.3390/cancers12082158
Submission received: 26 June 2020 / Revised: 31 July 2020 / Accepted: 2 August 2020 / Published: 4 August 2020
(This article belongs to the Special Issue Recent Advances on the Pathobiology and Treatment of Multiple Myeloma)

Abstract

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.
Keywords: multiple myeloma; MGUS; oncogenesis; plasma cells; endosteal niche; bone lesion; bone marrow microenvironment; cell-to-cell heterogeneity; gene expression noise multiple myeloma; MGUS; oncogenesis; plasma cells; endosteal niche; bone lesion; bone marrow microenvironment; cell-to-cell heterogeneity; gene expression noise

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MDPI and ACS Style

Capp, J.-P.; Bataille, R. Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory. Cancers 2020, 12, 2158. https://doi.org/10.3390/cancers12082158

AMA Style

Capp J-P, Bataille R. Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory. Cancers. 2020; 12(8):2158. https://doi.org/10.3390/cancers12082158

Chicago/Turabian Style

Capp, Jean-Pascal, and Régis Bataille. 2020. "Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory" Cancers 12, no. 8: 2158. https://doi.org/10.3390/cancers12082158

APA Style

Capp, J.-P., & Bataille, R. (2020). Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory. Cancers, 12(8), 2158. https://doi.org/10.3390/cancers12082158

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