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Editorial
. 2012 Oct 15;11(20):3715-7.
doi: 10.4161/cc.22178. Epub 2012 Sep 14.

The cellular architecture of multiple myeloma

Carolina Vicente-Dueñas, Isabel Romero-Camarero, Francisco Javier García-Criado, César Cobaleda, Isidro Sánchez-García
Editorial

The cellular architecture of multiple myeloma

Carolina Vicente-Dueñas et al. Cell Cycle. .
No abstract available

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Figures

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Figure 1. Cellular architecture and multiple myeloma (MM) development. (A) Current working model for the development of MM in humans. In the current view of the initiation and progression of MM, an initiating hit is required to immortalize a plasma cell. Such cells are then destined to acquire additional genetics hits over time. The acquisition of additional hits further deregulates the behavior of the plasma cells, thus leading to a subclonal genetic heterogeneity within tumor plasma cells. Specific subclones of tumor plasma cells may contribute to the initiation, treatment resistance or relapse. (B and C) A model by which ectopic expression of MafB reprogrammes HS/PCs into tumor plasma cells. This new model of MM development is based on the idea that initiating hits take place within stem/progenitor cells. These genetic or epigenetic changes would not interfere with normal B cell development, but become active in the process of terminal plasma cell differentiation, leading to the appearance of MM. According to this model, MM is the result of a cell reprogramming process, where genetically distinct MM stem cell subclones may exist on top of each tumor MM mass, revealing a highly complex cellular composition of MM. According to this model, the cellular types that compose the tumoral tissue include MM stem cells close to the terminal differentiated tumor plasma cells (B). The genetic heterogeneity can affect any cellular type of the MM tissue and any of the specific subclones of MM stem cells or tumor plasma cells may contribute to the different steps of the MM evolution before (B) and after treatment (C).
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Comment on

  • Vicente-Dueñas C, Romero-Camarero I, Gonzalez-Herrero I, Alonso-Escudero E, Abollo-Jimenez F, Jiang X, Gutierrez NC, Orfao A, Mari­n N, Villar LM, Criado MC, Pintado B, Flores T, Alonso-Lopez D, De Las Rivas J, Jimenez R, Criado FJ, Cenador MB, Lossos IS, Cobaleda C, Sanchez-Garcia I. A novel molecular mechanism involved in multiple myeloma development revealed by targeting MafB to haematopoietic progenitors. EMBO J. 2012;31:3704–17. doi: 10.1038/emboj.2012.227. doi: 10.1038/emboj.2012.227

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