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      Recent advances in the biology and treatment of brain metastases of non-small cell lung cancer: summary of a multidisciplinary roundtable discussion

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          Abstract

          This article is the result of a round table discussion held at the European Lung Cancer Conference (ELCC) in Geneva in May 2017. Its purpose is to explore and discuss the advances in the knowledge about the biology and treatment of brain metastases originating from non-small cell lung cancer. The authors propose a series of recommendations for research and treatment within the discussed context.

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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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            Incidence proportions of brain metastases in patients diagnosed (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System.

            Jill Barnholtz-Sloan, Andrew Sloan, Faith G. Davis … (2004)
            Population-based estimates of the incidence of brain metastases are not generally available. The purpose of this study was to calculate population-based incidence proportions (IPs) of brain metastases from single primary lung, melanoma, breast, renal, or colorectal cancer. Patients diagnosed with single primary lung, melanoma, breast, renal, or colorectal cancer (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System (MDCSS) were used for analysis. IP of brain metastases by primary site and variable of interest (race, sex, age at diagnosis of primary cancer, and Surveillance, Epidemiology, and End Results [SEER] stage of primary cancer) was calculated with 95% CIs. Total IP percentage (IP%) of brain metastases was 9.6% for all primary sites combined, and highest for lung (19.9%), followed by melanoma (6.9%), renal (6.5%), breast (5.1%), and colorectal (1.8%) cancers. Racial differences were seen with African Americans demonstrating higher IP% of brain metastases compared with other racial groups for most primary sites. IP% was significantly higher for female patients with lung cancer, and significantly higher for male patients with melanoma. The highest IP% of brain metastases occurred at different ages at diagnoses: age 40 to 49 years for primary lung cancer; age 50 to 59 years for primary melanoma, renal, or colorectal cancers; and age 20 to 39 for primary breast cancer. IP% significantly increased as SEER stage of primary cancer advanced for all primary sites. Total IP% of brain metastases was lower than previously reported, and it varied by primary site, race, sex, age at diagnosis of primary cancer, and SEER stage of primary cancer.
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              Carcinoma-astrocyte gap junctions promote brain metastasis by cGAMP transfer

              Qing Chen, Adrienne Boire, Xin Jin … (2016)
              SUMMARY Brain metastasis represents a substantial source of morbidity and mortality in various cancers, and is characterized by high resistance to chemotherapy. Here we define the role of the most abundant cell type in the brain, the astrocyte, in promoting brain metastasis. Breast and lung cancer cells express protocadherin 7 (PCDH7) to favor the assembly of carcinoma-astrocyte gap junctions composed of connexin 43 (Cx43). Once engaged with the astrocyte gap-junctional network, brain metastatic cancer cells employ these channels to transfer the second messenger cGAMP to astrocytes, activating the STING pathway and production of inflammatory cytokines IFNα and TNFα. As paracrine signals, these factors activate the STAT1 and NF-κB pathways in brain metastatic cells, which support tumour growth and chemoresistance. The orally bioavailable modulators of gap junctions meclofenamate and tonabersat break this paracrine loop, and we provide proof-of-principle for the applicability of this therapeutic strategy to treat established brain metastasis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): ESMO Open
                Journal ID (iso-abbrev): ESMO Open
                Journal ID (hwp): esmoopen
                Journal ID (publisher-id): esmoopen
                Title: ESMO Open
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Electronic): 2059-7029
                Publication date Collection: 2018
                Publication date (Electronic): 26 January 2018
                Volume: 3
                Issue: 1
                Electronic Location Identifier: e000262
                Affiliations
                [1 ] departmentClinical Division of Oncology, Department of Medicine I , Comprehensive Cancer Centre, Medical University Vienna – General Hospital , Vienna, Austria
                [2 ] Neurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg , Heidelberg, Germany
                [3 ] Clinical Cooperation Unit Neuro-oncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ) , Heidelberg, Germany
                [4 ] Brain Metastasis Group, Spanish National Cancer Research Centre (CNIO) , Madrid, Spain
                [5 ] departmentMedical Faculty Mannheim , University of Heidelberg , Mannheim, Baden-Württemberg, Germany
                [6 ] departmentRadiation Oncology Department, Radiobiology team 11, UMR1037 INSERM , Institut Universitaire du Cancer de Toulouse Oncopole, Centre de Recherche contre le Cancer , Toulouse, France
                [7 ] departmentDepartment of Neurosurgery , Medical University of Vienna (MUV) , Vienna, Austria
                [8 ] departmentDepartment of Neurosurgery , University of California San Francisco (UCSF) , San Francisco, USA
                [9 ] Comprehensive Cancer Center–Central Nervous System Tumours Unit (CCC-CNS), Medical University Vienna (MUV) , Vienna, Austria
                [10 ] departmentDepartment of Neurosurgery , Ludwig-Maximilians University, Munich-Grosshadern, Germany and German Cancer Consortium (DKTK) at the German Cancer Research Centre (DKFZ) , Heidelberg, Germany
                Author notes
                [Correspondence to ] Professor Matthias Preusser; matthias.preusser@ 123456meduniwien.ac.at
                Article
                Publisher ID: esmoopen-2017-000262
                DOI: 10.1136/esmoopen-2017-000262
                PMC ID: 5786916
                PubMed ID: 29387475
                SO-VID: ec8e0651-5cd1-415f-83a9-e90e1f3e7678
                Copyright © © European Society for Medical Oncology (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                Date received : 18 August 2017
                Date revision received : 21 November 2017
                Date accepted : 29 November 2017
                Categories
                Subject: Review
                Subject: 1506
                Custom metadata
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                Keywords: biology and treatment of brain
                Data availability:
                Keywords: biology and treatment of brain

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