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      Bone Marrow Microenvironment in Multiple Myeloma Progression

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          Abstract

          Substantial advances have been made in understanding the biology of multiple myeloma (MM) through the study of the bone marrow (BM) microenvironment. Indeed, the BM niche appears to play an important role in differentiation, migration, proliferation, survival, and drug resistance of the malignant plasma cells. The BM niche is composed of a cellular compartment (stromal cells, osteoblasts, osteoclasts, endothelial cells, and immune cells) and a noncellular compartment including the extracellular matrix (ECM) and the liquid milieu (cytokines, growth factors, and chemokines). In this paper we discuss how the interaction between the malignant plasma cell and the BM microenvironment allowed myeloma progression through cell homing and the new concept of premetastatic niche.

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          The metastatic niche: adapting the foreign soil.

          Bethan Psaila, David Lyden (2009)
          The 'seed and soil' hypothesis for metastasis sets forth the concept that a conducive microenvironment, or niche, is required for disseminating tumour cells to engraft distant sites. This Opinion presents emerging data that support this concept and outlines the potential mechanism and temporal sequence by which changes occur in tissues distant from the primary tumour. To enable improvements in the prognosis of advanced malignancy, early interventions that target both the disseminating seed and the metastatic soil are likely to be required.
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            Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets.

            Teru Hideshima, Constantine Mitsiades, Giovanni Tonon … (2007)
            Multiple myeloma is a plasma cell malignancy characterized by complex heterogeneous cytogenetic abnormalities. The bone marrow microenvironment promotes multiple myeloma cell growth and resistance to conventional therapies. Although multiple myeloma remains incurable, novel targeted agents, used alone or in combination, have shown great promise to overcome conventional drug resistance and improve patient outcome. Recent oncogenomic studies have further advanced our understanding of the molecular pathogenesis of multiple myeloma, providing the framework for new prognostic classification and identifying new therapeutic targets.
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              The role of Notch in tumorigenesis: oncogene or tumour suppressor?

              Freddy Radtke, Kenneth Raj (2003)
              Notch signalling participates in the development of multicellular organisms by maintaining the self-renewal potential of some tissues and inducing the differentiation of others. Involvement of Notch in cancer was first highlighted in human T-cell leukaemia, fuelling the notion that aberrant Notch signalling promotes tumorigenesis. However, there is mounting evidence that Notch signalling is not exclusively oncogenic. It can instead function as a tumour suppressor.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Biomed Biotechnol
                Journal ID (iso-abbrev): J. Biomed. Biotechnol
                Journal ID (publisher-id): JBB
                Title: Journal of Biomedicine and Biotechnology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1110-7243
                ISSN (Electronic): 1110-7251
                Publication date (Print): 2012
                Publication date (Electronic): 3 October 2012
                Volume: 2012
                Electronic Location Identifier: 157496
                Affiliations
                1Dana-Farber Cancer Institute, Department of Medical Oncology, Harvard Medical School, 450 Brookline Avnue, HIM 246, Boston, MA 02215, USA
                2Service des Maladies du Sang, CHRU de Lille, 59000 Lille, France
                Author notes

                Academic Editor: Sue-Hwa Lin

                Article
                DOI: 10.1155/2012/157496
                PMC ID: 3471001
                PubMed ID: 23093834
                SO-VID: e7952c75-1adb-4bad-9b96-a054f8d4b019
                Copyright © Copyright © 2012 S. Manier et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 3 August 2012
                Date accepted : 18 September 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
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                ScienceOpen disciplines: Molecular medicine

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