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      The challenge of targeting metastasis

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          Abstract

          Metastases that are resistant to conventional therapy are the major cause of death from cancer. In most patients, metastasis has already occurred by the time of diagnosis. Thus, the prevention of metastasis is unlikely to be of therapeutic benefit. The biological heterogeneity of metastases presents a major obstacle to treatment. However, the growth and survival of metastases depend on interactions between tumor cells and host homeostatic mechanisms. Targeting these interactions, in addition to the tumor cells, can produce synergistic therapeutic effects against existing metastases.

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          Microenvironmental regulation of metastasis.

          Johanna A. Joyce, Jeffrey W Pollard (2009)
          Metastasis is a multistage process that requires cancer cells to escape from the primary tumour, survive in the circulation, seed at distant sites and grow. Each of these processes involves rate-limiting steps that are influenced by non-malignant cells of the tumour microenvironment. Many of these cells are derived from the bone marrow, particularly the myeloid lineage, and are recruited by cancer cells to enhance their survival, growth, invasion and dissemination. This Review describes experimental data demonstrating the role of the microenvironment in metastasis, identifies areas for future research and suggests possible new therapeutic avenues.
          Article 0 comments Cited 1213 times – based on 0 reviews     Review now
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            Genes that mediate breast cancer metastasis to the brain.

            Paula Bos, Xiang Zhang, Cristina Nadal … (2009)
            The molecular basis for breast cancer metastasis to the brain is largely unknown. Brain relapse typically occurs years after the removal of a breast tumour, suggesting that disseminated cancer cells must acquire specialized functions to take over this organ. Here we show that breast cancer metastasis to the brain involves mediators of extravasation through non-fenestrated capillaries, complemented by specific enhancers of blood-brain barrier crossing and brain colonization. We isolated cells that preferentially infiltrate the brain from patients with advanced disease. Gene expression analysis of these cells and of clinical samples, coupled with functional analysis, identified the cyclooxygenase COX2 (also known as PTGS2), the epidermal growth factor receptor (EGFR) ligand HBEGF, and the alpha2,6-sialyltransferase ST6GALNAC5 as mediators of cancer cell passage through the blood-brain barrier. EGFR ligands and COX2 were previously linked to breast cancer infiltration of the lungs, but not the bones or liver, suggesting a sharing of these mediators in cerebral and pulmonary metastases. In contrast, ST6GALNAC5 specifically mediates brain metastasis. Normally restricted to the brain, the expression of ST6GALNAC5 in breast cancer cells enhances their adhesion to brain endothelial cells and their passage through the blood-brain barrier. This co-option of a brain sialyltransferase highlights the role of cell-surface glycosylation in organ-specific metastatic interactions.
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              Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis.

              John M L Ebos, Christina R Lee, William Cruz-Munoz … (2009)
              Herein we report that the VEGFR/PDGFR kinase inhibitor sunitinib/SU11248 can accelerate metastatic tumor growth and decrease overall survival in mice receiving short-term therapy in various metastasis assays, including after intravenous injection of tumor cells or after removal of primary orthotopically grown tumors. Acceleration of metastasis was also observed in mice receiving sunitinib prior to intravenous implantation of tumor cells, suggesting possible "metastatic conditioning" in multiple organs. Similar findings with additional VEGF receptor tyrosine kinase inhibitors implicate a class-specific effect for such agents. Importantly, these observations of metastatic acceleration were in contrast to the demonstrable antitumor benefits obtained when the same human breast cancer cells, as well as mouse or human melanoma cells, were grown orthotopically as primary tumors and subjected to identical sunitinib treatments.
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                Author and article information

                Contributors
                Isaiah J. Fidler: ifidler@mdanderson.org
                Journal
                Journal ID (nlm-ta): Cancer Metastasis Rev
                Journal ID (iso-abbrev): Cancer Metastasis Rev
                Title: Cancer Metastasis Reviews
                Publisher: Springer US (New York )
                ISSN (Print): 0167-7659
                ISSN (Electronic): 1573-7233
                Publication date (Electronic): 2 September 2015
                Publication date PMC-release: 2 September 2015
                Publication date (Print): 2015
                Volume: 34
                Issue: 4
                Pages: 635-641
                Affiliations
                [ ]Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 173, Houston, TX 77030 USA
                [ ]Department of Immunology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 173, Houston, TX 77030 USA
                Article
                Publisher ID: 9586
                DOI: 10.1007/s10555-015-9586-9
                PMC ID: 4661188
                PubMed ID: 26328524
                SO-VID: 39ac0c59-4b0f-4448-97b9-4d12ead07916
                Copyright © © The Author(s) 2015
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Categories
                Subject: Non-Thematic Review
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media New York 2015

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: biologic heterogeneity,genetic instability,organ microenvironment,metastasis progenitor cell
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: biologic heterogeneity, genetic instability, organ microenvironment, metastasis progenitor cell

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