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  • 1. Frentzas, Sophia
    et al.
    Simoneau, Eve
    Bridgeman, Victoria L.
    Vermeulen, Peter B.
    Foo, Shane
    Kostaras, Eleftherios
    Nathan, Mark R.
    Wotherspoon, Andrew
    Gao, Zu-Hua
    Shi, Yu
    Van den Eynden, Gert
    Daley, Frances
    Peckitt, Clare
    Tan, Xianming
    Salman, Ayat
    Lazaris, Anthoula
    Gazinska, Patrycja
    Berg, Tracy J.
    Eltahir, Zak
    Ritsma, Laila
    van Rheenen, Jacco
    Khashper, Alla
    Brown, Gina
    Nyström, Hanna
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Van Laere, Steven
    Loyer, Evelyne
    Dirix, Luc
    Cunningham, David
    Metrakos, Peter
    Reynolds, Andrew R.
    Vessel co-option mediates resistance to anti-angiogenic therapy in liver metastases2016In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 22, no 11, p. 1294-1302Article in journal (Refereed)
    Abstract [en]

    The efficacy of angiogenesis inhibitors in cancer is limited by resistance mechanisms that are poorly understood. Notably, instead of through the induction of angiogenesis, tumor vascularization can occur through the nonangiogenic mechanism of vessel co-option. Here we show that vessel co-option is associated with a poor response to the anti-angiogenic agent bevacizumab in patients with colorectal cancer liver metastases. Moreover, we find that vessel co-option is also prevalent in human breast cancer liver metastases, a setting in which results with anti-angiogenic therapy have been disappointing. In preclinical mechanistic studies, we found that cancer cell motility mediated by the actin-related protein 2/3 complex (Arp2/3) is required for vessel co-option in liver metastases in vivo and that, in this setting, combined inhibition of angiogenesis and vessel co-option is more effective than the inhibition of angiogenesis alone. Vessel co-option is therefore a clinically relevant mechanism of resistance to anti-angiogenic therapy and combined inhibition of angiogenesis and vessel co-option might be a warranted therapeutic strategy.

  • 2.
    Gerold, Gisa
    et al.
    Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York, USA.
    Rice, Charles M
    Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York, USA.
    Locking out hepatitis C2011In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 17, no 5, p. 542-4Article in journal (Refereed)
  • 3. Movérare-Skrtic, Sofia
    et al.
    Henning, Petra
    Liu, Xianwen
    Nagano, Kenichi
    Saito, Hiroaki
    Börjesson, Anna E.
    Sjögren, Klara
    Windahl, Sara H.
    Farman, Helen
    Kindlund, Bert
    Engdahl, Cecilia
    Koskela, Antti
    Zhang, Fu-Ping
    Eriksson, Emma E.
    Zaman, Farasat
    Hammarstedt, Ann
    Isaksson, Hanna
    Bally, Marta
    Kassem, Ali
    Umeå University, Faculty of Medicine, Department of Odontology.
    Lindholm, Catharina
    Sandberg, Olof
    Aspenberg, Per
    Sävendahl, Lars
    Feng, Jian Q.
    Tuckermann, Jan
    Tuukkanen, Juha
    Poutanen, Matti
    Baron, Roland
    Lerner, Ulf H
    Umeå University, Faculty of Medicine, Department of Odontology. Centre for Bone and Arthritis Research at Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Gori, Francesca
    Ohlsson, Claes
    Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures2014In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 20, no 11, p. 1279-1288Article in journal (Refereed)
    Abstract [en]

    The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need.

  • 4.
    Nilsson, Emma C
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Storm, Rickard J
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Bauer, Johannes
    University of Tübingen.
    Johansson, Susanne M C
    Umeå University, Faculty of Science and Technology, Department of Chemistry. Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Lookene, Aivar
    Tallinn University of Technology, Tallinn, Estonia..
    Ångström, Jonas
    University of Göteborg.
    Hedenström, Mattias
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Eriksson, Therese L
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Frängsmyr, Lars
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Rinaldi, Simon
    University of Glasgow.
    Willison, Hugh J
    University of Glasgow.
    Domellöf, Fatima Pedrosa
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Ophthalmology. Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
    Stehle, Thilo
    University of Tübingen, Vanderbilt University School of Medicine.
    Arnberg, Niklas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology. Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS).
    The GD1a glycan is a cellular receptor for adenoviruses causing epidemic keratoconjunctivitis (Letter)2011In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 17, no 1, p. 105-109Article in journal (Refereed)
    Abstract [en]

    Adenovirus type 37 (Ad37) is a leading cause of epidemic keratoconjunctivitis (EKC), a severe and highly contagious ocular disease. Whereas most other adenoviruses infect cells by engaging CD46 or the coxsackie and adenovirus receptor (CAR), Ad37 binds previously unknown sialic acid-containing cell surface molecules. By glycan array screening, we show here that the receptor-recognizing knob domain of the Ad37 fiber protein specifically binds a branched hexasaccharide that is present in the GD1a ganglioside and that features two terminal sialic acids. Soluble GD1a glycan and GD1a-binding antibodies efficiently prevented Ad37 virions from binding and infecting corneal cells. Unexpectedly, the receptor is constituted by one or more glycoproteins containing the GD1a glycan motif rather than the ganglioside itself, as shown by binding, infection and flow cytometry experiments. Molecular modeling, nuclear magnetic resonance and X-ray crystallography reveal that the two terminal sialic acids dock into two of three previously established sialic acid-binding sites in the trimeric Ad37 knob. Surface plasmon resonance analysis shows that the knob-GD1a glycan interaction has high affinity. Our findings therefore form a basis for the design and development of sialic acid-containing antiviral drugs for topical treatment of EKC.

  • 5.
    Urban, Constantin
    et al.
    Department of Cellular Microbiology, Max Planck Institute for Infection Biology, Charitéplatz 1, Berlin 10117, Germany.
    Zychlinsky, Arturo
    Department of Cellular Microbiology, Max Planck Institute for Infection Biology, Charitéplatz 1, Berlin 10117, Germany.
    Netting bacteria in sepsis2007In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 13, no 4, p. 403-404Article in journal (Other academic)
  • 6. Van Hoecke, Annelies
    et al.
    Schoonaert, Lies
    Lemmens, Robin
    Timmers, Mieke
    Staats, Kim A.
    Laird, Angela S.
    Peeters, Elke
    Philips, Thomas
    Goris, An
    Dubois, Benedicte
    Andersen, Peter M.
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Neuroscience.
    Al-Chalabi, Ammar
    Thijs, Vincent
    Turnley, Ann M.
    van Vught, Paul W.
    Veldink, Jan H.
    Hardiman, Orla
    Van Den Bosch, Ludo
    Gonzalez-Perez, Paloma
    Van Damme, Philip
    Brown, Robert H., Jr.
    van den Berg, Leonard H.
    Robberecht, Wim
    EPHA4 is a disease modifier of amyotrophic lateral sclerosis in animal models and in humans2012In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 18, no 9, p. 1418-Article in journal (Refereed)
    Abstract [en]

    Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting motor neurons. Disease onset and progression are variable, with survival ranging from months to decades. Factors underlying this variability may represent targets for therapeutic intervention. Here, we have screened a zebrafish model of ALS and identified Epha4, a receptor in the ephrin axonal repellent system, as a modifier of the disease phenotype in fish, rodents and humans. Genetic as well as pharmacological inhibition of Epha4 signaling rescues the mutant SOD1 phenotype in zebrafish and increases survival in mouse and rat models of ALS. Motor neurons that are most vulnerable to degeneration in ALS express higher levels of Epha4, and neuromuscular re-innervation by axotomized motor neurons is inhibited by the presence of Epha4. In humans with ALS, EPHA4 expression inversely correlates with disease onset and survival, and loss-of-function mutations in EPHA4 are associated with long survival. Furthermore, we found that knockdown of Epha4 also rescues the axonopathy induced by expression of mutant TAR DNA-binding protein 43 (TDP-43), another protein causing familial ALS, and the axonopathy induced by knockdown of survival of motor neuron 1, a model for spinomuscular atrophy. This suggests that Epha4 generically modulates the vulnerability of (motor) neurons to axonal degeneration and may represent a new target for therapeutic intervention.

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