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  • 1
    In: Neuro-Oncology, 2014, Vol. 16(12), pp.1565-1566
    Description: See the article by Kim et al, on pages 1585–1598.
    Keywords: Medicine;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 2
    Language: English
    In: Nature, August 2018, Vol.560(7716), pp.35-36
    Description: Certain cancers are prone to invade the nervous system, which leads to poorer prognosis. A study of leukaemia in mice reveals an unexpectedly direct invasion route from the bone marrow to the central nervous system. Certain cancers are prone to invade the nervous system, which leads to poorer prognosis. A study of leukaemia in mice reveals an unexpectedly direct invasion route from the bone marrow to the central nervous system.
    Keywords: Cancer ; Medical Research ; Neuroscience ; Central Nervous System ; Leukemia
    ISSN: 00280836
    E-ISSN: 1476-4687
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  • 3
    Language: English
    In: Science (New York, N.Y.), 09 March 2018, Vol.359(6380), pp.1100-1101
    Description: Communication in networks is the basis of many social and biological functions. Recent findings have added an uncomfortable twist to this view: Tumors can function as communicating networks, too. In several malignancies such as incurable brain tumors, long protrusions extend from cancer cells, connecting...
    Keywords: Cell Communication ; Brain Neoplasms -- Pathology ; Cell Surface Extensions -- Pathology ; Glioblastoma -- Pathology
    ISSN: 00368075
    E-ISSN: 1095-9203
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  • 4
    Article
    Article
    Language: English
    In: Journal of Molecular Medicine, 2015, Vol.93(11), pp.1213-1220
    Description: Metastasizing cancer cells that arrest in brain microvessels have to face an organ microenvironment that is alien, and exclusive. In order to survive and thrive in this foreign soil, the malignant cells need to successfully master a sequence of steps that includes close interactions with pre-existing brain microvessels, and other nonmalignant cell types. Unfortunately, a relevant number of circulating cancer cells is capable of doing so: brain metastasis is a frequent and devastating complication of solid tumors, becoming ever more important in times where the systemic tumor disease is better controlled and life of cancer patients is prolonged. Thus, it is very important to understand which environmental cues are necessary for effective brain colonization. This review gives an overview of the niches we know, including those who govern cancer cell dormancy, survival, and proliferation in the brain. Colonization of pre-existing niches related to stemness and resistance is a hallmark of successful brain metastasis. A deeper understanding of those host factors can help to identify the most vulnerable steps of the metastatic cascade, which might be most amenable to therapeutic interventions.
    Keywords: Brain ; Metastasis ; Metastases ; Blood-brain barrier ; Perivascular ; Niche
    ISSN: 0946-2716
    E-ISSN: 1432-1440
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  • 5
    In: Journal of Pathology, July 2017, Vol.242(3), pp.267-272
    Description: An increasing body of evidence suggests that solid tumours do not require the generation of new blood vessels, i.e. angiogenesis, to successfully grow, and to colonize normal tissue. Instead, many tumour cells make the best use of what they find: pre‐existing blood vessels of the host. In these cases, the host vasculature is incorporated by the growing tumour, resulting in a new organ consisting of malignant and non‐malignant cell types. In consequence, pre‐existing vessels are exploited by the tumour for optimal access to oxygen and nutrients. In this perspective article, the argument is made that tumour cells might gain even more: that is, access to the very special microenvironment of the perivascular niche. Here, specific cues for invasion, metastasis, survival, stem‐like features, dormancy and, potentially, also immune escape exist – for non‐malignant and malignant cells alike. The consequence of the hijacking of normal blood vessels and their perivascular niches by tumours is that antiangiogenic agents have little chance to work, and that tumour cells are better protected from the adverse effects of cytotoxic and targeted therapies. Thus, disturbing vascular hijacking could make tumours less resistant to established therapies. Concepts of how to do this are just starting to be explored. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Keywords: Vascular Co‐Option ; Angiocentric Growth ; Perivascular Niche ; Angiogenesis
    ISSN: 0022-3417
    E-ISSN: 1096-9896
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  • 6
    Language: English
    In: Brain Research, Feb 25, 2013, Vol.1497, p.85(16)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2012.12.024 Byline: Marie Paus (a), Zacharias Kohl (a), Nada M.-B. Ben Abdallah (a), Dagmar Galter (c), Frank Gillardon (b), Jurgen Winkler (a) Keywords: Parkinson's disease; Leucine-rich repeat kinase 2; Neurogenesis; Doublecortin; Neurite outgrowth; Mossy fibers Abbreviations: BrdU, 5-Bromo-2-Deoxyuridine; CA3, Cornus Ammonis 3 region of the hippocampus; COR, C-terminal of Roc; CPS, Cryoprotectant Solution; DAB, 3,3-Diaminobenzidine; DCX, Doublecortin; DG, Dentate Gyrus; GABA, Gamma-Amino-Butyric-Acid; IIP MFs, Intra-Infra-Pyramidal Mossy Fibers; i.p., Intraperitoneal; KO, Knockout; LRR, Leucin-Rich-Repeat; LRRK2, Leucin-Rich-Repeat Kinase 2; MAP, Microtubule Associated Protein; MAPKKK, Mitogen-Activated Protein Kinase Kinase Kinase; NaCl, Natriumchloride; NeuN, Neuronal Specific Nuclear Protein; NPC, Neuronal Precursor Cell; NSC, Neuronal Stem Cell; OB, Olfactory Bulb; PB, Phosphate Buffer; PBS, Phosphate Buffered Saline; PD, Parkinson's Disease; PFA, Paraformaldehyde; Roc, Ras in complex protein; ROI, Region of Interest; SEM, Standard Error of the Mean; SGZ, Subgranular Zone; SN, Substantia Nigra; SP MFs, Supra-Pyramidal Mossy Fibers; SVZ, Subventricular Zone; TBS, Tris Buffered Saline; WT, Wildtype; ZnT-3, Zink-Transporter-3 Abstract: Adult neurogenesis, the formation of new neurons in the mammalian forebrain, is one important mechanism maintaining lifelong neuronal plasticity. The generation and maturation of adult neural stem and progenitor cells is impaired in models of neurodegenerative diseases, in particular Parkinson's disease (PD). Monogenetic forms of PD were identified and associated with several genes including the leucine-rich-repeat kinase 2 (LRRK2). Some of the underlying mechanisms in neurodegenerative diseases are closely linked to neuronal plasticity, and induce changes in adult neurogenesis, neuritic maintenance, synaptic transmission, and neural connectivity. We investigated adult neurogenesis and neuritic development of newly formed neurons in the hippocampal dentate gyrus of LRRK2 knockout mice. Proliferation and survival of newly generated cells were unchanged. However, the expression profile of maturation markers in surviving newly generated cells was altered. While immature neuronal phenotypes were significantly increased, the mature neuronal phenotype of surviving cells remained unchanged. Importantly, the absolute number of immature doublecortin positive neuroblasts was significantly increased in the hippocampus of LRRK2 knockout mice. These neuroblasts presented extended dendritic length with a more complex arborization. Furthermore, LRRK2 deletion resulted in an increased volume of the axonal mossy fiber bundle projecting from dentate granule cells to CA3 pyramidal neurons. Our findings suggest that LRRK2 influences neurogenesis and particularly neuronal morphogenesis. As neurogenesis and the pre-/post- synaptic compartments are significantly altered in PD, our data advance LRRK2 as a potent candidate in addressing neuroregenerative processes. Author Affiliation: (a) Department of Molecular Neurology, University Hospital Erlangen, Erlangen, Germany (b) Boehringer Ingelheim Pharma GmbH Co. KG, Ingelheim, Germany (c) Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden Article History: Accepted 13 December 2012
    Keywords: Nervous System Diseases -- Analysis ; Neurosciences -- Analysis ; Neurons -- Analysis ; Stem Cells -- Analysis ; Phosphates -- Analysis ; Parkinson Disease -- Analysis ; Gaba -- Analysis
    ISSN: 0006-8993
    Source: Cengage Learning, Inc.
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  • 7
    Language: English
    In: Cancer Research, 04/15/2013, Vol.73(8 Supplement), pp.3916-3916
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 8
    Article
    Article
    Language: English
    In: Handbook of clinical neurology, 2018, Vol.149, pp.43-56
    Description: Metastasis to the brain is an increasing complication of solid cancers. Fortunately, our understanding of its pathogenesis has greatly increased in the last decade, with crucial insights into the molecular and cellular determinants of successful brain colonization; some aspects remain less well understood. The latter include the exact features of brain metastasis-initiating cancer cells, and a potential premetastatic niche. It is clear that a brain-arrested cancer cell has to master a sequence of steps to eventually grow to a clinically relevant brain metastasis. Various brain-specific cell types and molecular niches promote or hinder brain colonization in a dynamic and reciprocal manner. After mandatory extravasation and colonization of a brain-specific perivascular niche, the cancer cell can stay dormant, or further grow by dynamic interactions with cerebral blood vessels. In addition, the activation of certain molecular pathways on site of the cancer cell which are related to growth, motility, survival, and adaptation to the brain environment appears also important, given their characteristic modification in brain metastases of patients. A deeper understanding of the most vulnerable steps of the brain metastatic cascade may foster the development of novel preventive approaches, and that of core biologic mechanisms for macrometastatic growth and persistence will help to develop better therapeutics.
    Keywords: Angiogenesis ; Astrocytes ; Biology ; Blood Vessels ; Brain Metastases ; Cancer Stem Cells ; Endothelial Cells ; Metastatic Cascade ; Microglia ; Perivascular Niche ; Brain Neoplasms ; Neoplasm Metastasis ; Neoplasms -- Pathology
    ISSN: 0072-9752
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 9
    Article
    Article
    BMJ Publishing Group Ltd
    Language: English
    In: ESMO Open, 19 December 2016, Vol.1(6)
    Description: In this podcast, a new biological insight in brain tumours is discussed. The author's group has identified the existence of a tumour cell network in incurable gliomas which facilitates multicellular communication and exchange of small molecules between single tumour cells. The tumour cells that are integrated in this network, around 50% of cells according to studies in mouse models and patient samples, appear to be protected from the effects of radiotherapy and possibly also chemotherapy, which may explain how such tumours develop resistance to therapies and why patients relapse after treatment. An overview of ideas that are being investigated preclinically to therapeutically target this network of tumour cells is given. These include approaches to disrupt the network, such as obstructing cellular communication with gap junction blockers and targeting the neurodevelopmental pathways required to form the networks. Conversely, methods to exploit the network through the local application of gap junction-permeable drugs that specifically target the integrated tumour cells could also being studied. This new discovery may result in the development of therapeutic strategies which the author hopes will reach the clinic in the next few years.
    Keywords: Podcast
    E-ISSN: 2059-7029
    E-ISSN: 20597029
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  • 10
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States, Sept 3, 2013, Vol.110(36), p.14735(6)
    Description: Disruption of the blood--brain barrier (BBB) is a hallmark of acute inflammatory lesions in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis. This disruption may precede and facilitate the infiltration of encephalitogenic T cells. The signaling events that lead to this BBB disruption are incompletely understood but appear to involve dysregulation of tight-junction proteins such as claudins. Pharmacological interventions aiming at stabilizing the BBB in MS might have therapeutic potential. Here, we show that the orally available small molecule LY-317615, a synthetic bisindolylmaleimide and inhibitor of protein kinase C[beta], which is clinically under investigation for the treatment of cancer, suppresses the transmigration of activated T cells through an inflamed endothelial cell barrier, where it leads to the induction of the tight-junction molecules zona occludens-1, claudin 3, and claudin 5 and other pathways critically involved in transendothelial leukocyte migration. Treatment of mice with ongoing experimental autoimmune encephalomyelitis with LY-317615 ameliorates inflammation, demyelination, axonal damage, and clinical symptoms. Although LY-317615 dose-dependently suppresses T-cell proliferation and cytokine production independent of antigen specificity, its therapeutic effect is abrogated in a mouse model requiring pertussis toxin. This abrogation indicates that the anti-inflammatory and clinical efficacy is mainly mediated by stabilization of the BBB, thus suppressing the transmigration of encephalitogenic T cells. Collectively, our data suggest the involvement of endothelial protein kinase C[beta] in stabilizing the BBB in autoimmune neuroinflammation and imply a therapeutic potential of BBB-targeting agents such as LY-317615 as therapeutic approaches for MS. EAE | enzastaurin | CNS www.pnas.org/cgi/doi/10.1073/pnas.1302569110
    Keywords: Protein Kinases -- Physiological Aspects ; Protein Kinases -- Health Aspects ; Blood-brain Barrier -- Physiological Aspects ; Blood-brain Barrier -- Health Aspects ; Encephalomyelitis -- Physiological Aspects
    ISSN: 0027-8424
    E-ISSN: 10916490
    Source: Cengage Learning, Inc.
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