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      The microenvironmental landscape of brain tumors

      research-article
      Author(s): 1 , 2 , 3
      Publication date PMC-release:
      Journal: Cancer cell

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          Abstract

          The brain tumor microenvironment (TME) is emerging as a critical regulator of cancer progression in primary and metastatic brain malignancies. The unique properties of this organ require a specific framework for designing TME-targeted interventions. Here we discuss a number of these distinct features, including brain-resident cell types, the blood-brain barrier, and various aspects of the immune-suppressive environment. We also highlight recent advances in therapeutically targeting the brain TME in cancer. By developing a comprehensive understanding of the complex and interconnected microenvironmental landscape of brain malignancies we will greatly expand the range of therapeutic strategies available to target these deadly diseases.

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          Neutrophils in cancer: neutral no more.

          Seth Coffelt, Max Wellenstein, Karin E de Visser (2016)
          Neutrophils are indispensable antagonists of microbial infection and facilitators of wound healing. In the cancer setting, a newfound appreciation for neutrophils has come into view. The traditionally held belief that neutrophils are inert bystanders is being challenged by the recent literature. Emerging evidence indicates that tumours manipulate neutrophils, sometimes early in their differentiation process, to create diverse phenotypic and functional polarization states able to alter tumour behaviour. In this Review, we discuss the involvement of neutrophils in cancer initiation and progression, and their potential as clinical biomarkers and therapeutic targets.
          Article 0 comments Cited 759 times – based on 0 reviews     Review now
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            Regression of Glioblastoma after Chimeric Antigen Receptor T-Cell Therapy.

            Christine E. Brown, Darya Alizadeh, Renate Starr … (2016)
            A patient with recurrent multifocal glioblastoma received chimeric antigen receptor (CAR)-engineered T cells targeting the tumor-associated antigen interleukin-13 receptor alpha 2 (IL13Rα2). Multiple infusions of CAR T cells were administered over 220 days through two intracranial delivery routes - infusions into the resected tumor cavity followed by infusions into the ventricular system. Intracranial infusions of IL13Rα2-targeted CAR T cells were not associated with any toxic effects of grade 3 or higher. After CAR T-cell treatment, regression of all intracranial and spinal tumors was observed, along with corresponding increases in levels of cytokines and immune cells in the cerebrospinal fluid. This clinical response continued for 7.5 months after the initiation of CAR T-cell therapy. (Funded by Gateway for Cancer Research and others; ClinicalTrials.gov number, NCT02208362 .).
            Article 0 comments Cited 727 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.
              Article 0 comments Cited 677 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101130617
                Journal ID (pubmed-jr-id): 29778
                Journal ID (nlm-ta): Cancer Cell
                Journal ID (iso-abbrev): Cancer Cell
                Title: Cancer cell
                ISSN (Print): 1535-6108
                ISSN (Electronic): 1878-3686
                Publication date Nihms-submitted: 17 March 2017
                Publication date (Print): 13 March 2017
                Publication date PMC-release: 13 March 2018
                Volume: 31
                Issue: 3
                Pages: 326-341
                Affiliations
                [1 ]Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC H3A 1A3, Canada
                [2 ]Ludwig Institute for Cancer Research, University of Lausanne, 1066 Lausanne, Switzerland
                [3 ]Department of Oncology, University of Lausanne, 1066 Lausanne, Switzerland
                Author notes
                [* ]Correspondence should be addressed to: Johanna A. Joyce, University of Lausanne, Chemin des Boveresses 155, Lausanne 1066, Switzerland, Phone: +41 21 6925937, Fax: +41 21 6925995, johanna@ 123456joycelab.org
                Article
                Accession ID: PMC5424263 Pmcid ID: PMC5424263 Pmc-uid ID: 5424263 Manuscript ID: nihpa854681
                DOI: 10.1016/j.ccell.2017.02.009
                PMC ID: 5424263
                PubMed ID: 28292436
                SO-VID: fee86573-f7f0-4dd0-9fcb-a115593a64ee
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