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      Understanding the Progression of Bone Metastases to Identify Novel Therapeutic Targets

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          Abstract

          Bone is one of the most preferential target site for cancer metastases, particularly for prostate, breast, kidney, lung and thyroid primary tumours. Indeed, numerous chemical signals and growth factors produced by the bone microenvironment constitute factors promoting cancer cell invasion and aggression. After reviewing the different theories proposed to provide mechanism for metastatic progression, we report on the gene expression profile of bone-seeking cancer cells. We also discuss the cross-talk between the bone microenvironment and invading cells, which impacts on the tumour actions on surrounding bone tissue. Lastly, we detail therapies for bone metastases. Due to poor prognosis for patients, the strategies mainly aim at reducing the impact of skeletal-related events on patients’ quality of life. However, recent advances have led to a better understanding of molecular mechanisms underlying bone metastases progression, and therefore of novel therapeutic targets.

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          Most cited references 143

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          Microenvironmental regulation of tumor progression and metastasis.

          Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
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            The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited.

             ISAIAH FIDLER (2003)
            Researchers have been studying metastasis for more than 100 years, and only recently have we gained insight into the mechanisms by which metastatic cells arise from primary tumours and the reasons that certain tumour types tend to metastasize to specific organs. Stephen Paget's 1889 proposal that metastasis depends on cross-talk between selected cancer cells (the 'seeds') and specific organ microenvironments (the 'soil') still holds forth today. It is now known that the potential of a tumour cell to metastasize depends on its interactions with the homeostatic factors that promote tumour-cell growth, survival, angiogenesis, invasion and metastasis. How has this field developed over the past century, and what major breakthroughs are most likely to lead to effective therapeutic approaches?
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              A genetic model for colorectal tumorigenesis

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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                04 January 2018
                January 2018
                : 19
                : 1
                Affiliations
                [1 ]Centre National de la Recherche Scientifique (CNRS), Université Côte d’Azur, Inserm, iBV, 06108 Nice, France; Annie.SCHMID-ALLIANA@ 123456unice.fr (A.S.-A.); Heidy.SCHMID-ANTOMARCHI@ 123456unice.fr (H.S.-A.); rasha.al-sahlanee@ 123456unice.fr (R.A.-S.); Patricia.Lagadec@ 123456unice.fr (P.L.); jean-claude.scimeca@ 123456unice.fr (J.-C.S.)
                [2 ]College of Sciences, Biotechnology Department, University of Bagdad, Bagdad, Iraq
                [3 ]Regenerative Medicine and Skeleton. RMeS-Lab, INSERM UMR 1229, University of Nantes, 44000 Nantes, France
                [4 ]Chimie et Interdisciplinarité, Synthèse, Analyse, Modélisation (CEISAM), UMR CNRS 6230, University of Nantes, 44300 Nantes, France
                [5 ]Faculty of Pharmaceutical Sciences, University of Nantes, 44000 Nantes, France
                Author notes
                [* ]Correspondence: elise.verron@ 123456univ-nantes.fr ; Tel.: +33-2-53-48-43-05
                [†]

                Contributed equally to this manuscript.

                Article
                ijms-19-00148
                10.3390/ijms19010148
                5796097
                29300334
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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