ArticleCancers2020
Multiple Myeloma as a Bone Disease? The Tissue Disruption-Induced Cell Stochasticity (TiDiS) Theory.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Cement Use in Bipolar Hemiarthroplasty and Its Association With Cancer Risk.Journal of Korean medical science · 2026Observational
- Evidence of Epigenetic Oncogenesis: A Turning Point in Cancer Research.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- An overview of multiple myeloma: A monoclonal plasma cell malignancy's diagnosis, management, and treatment modalities.Saudi journal of biological sciences · 2024Review
- The Ins and Outs of Endosteal Niche Disruption in the Bone Marrow: Relevance for Myeloma Oncogenesis.Biology · 2023Article
- Article
- Review
- Does Cancer Biology Rely on Parrondo's Principles?Cancers · 2021Review
- Group phenotypic composition in cancer.eLife · 2021Review
- Treatment Strategies Considering Micro-Environment and Clonal Evolution in Multiple Myeloma.Cancers · 2021Review
- A Similar Speciation Process Relying on Cellular Stochasticity in Microbial and Cancer Cell Populations.iScience · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.