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  1. AU="Biddlestone-Thorpe, Laura"
  2. AU="Townson, Andrea"
  3. AU="Mengliang Ye"
  4. AU=Tosi Gian Marco
  5. AU=Zaffran Stephane
  6. AU=Major E O
  7. AU=Szoka Lukasz
  8. AU="Karlsen, Allan E"
  9. AU="Andrea Russo"
  10. AU="Yang, Liuliu"
  11. AU="Holm, Liisa"
  12. AU="Montani, Rosana S"
  13. AU=Zhou Peiyuan AU=Zhou Peiyuan
  14. AU="Rachel Rossiter"
  15. AU="Hiovain-Asikainen, Katri"
  16. AU="Zehl, Martin"
  17. AU="Schmidt, Joel T"
  18. AU="Nguyen Quoc Hung"
  19. AU="Lucia Landoni"
  20. AU="Singh, Pawan"
  21. AU=Bevan D R
  22. AU="Arobindu Dash"
  23. AU="Xu, Boqi"
  24. AU="Minako Kamimoto"
  25. AU="Akinwunmi, Adebowale F"
  26. AU="Luo, Dong Dong"
  27. AU=Cao Jun
  28. AU="Lauren A Holt"
  29. AU="Nathalie Turgeon"
  30. AU="Santos, Bryan" AU="Santos, Bryan"
  31. AU="Platanios, Emmanouil Antonios"
  32. AU="Havva Keskin"
  33. AU="Gomis, Susantha"
  34. AU="Castro, Vanda"
  35. AU="Josiah, S M"
  36. AU="Yanjun Guo"
  37. AU="Klapp, Sabine H L"
  38. AU="Cipolat, Lauriane"
  39. AU="Rhee, Hwanseok"
  40. AU="El-Khatabi, K"
  41. AU="Lee, Seung Hee"
  42. AU=Torres Antoni
  43. AU="Baldacini, Mathieu"
  44. AU="Stahl, Alexander"
  45. AU="Karimbumkara, Seena Narayanan"
  46. AU="Welz Mirosław"
  47. AU="Jintao Ding"
  48. AU="Mei-Fang Chen"

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  1. Artikel ; Online: Nanomaterial-mediated CNS delivery of diagnostic and therapeutic agents.

    Biddlestone-Thorpe, Laura / Marchi, Nicola / Guo, Kathy / Ghosh, Chaitali / Janigro, Damir / Valerie, Kristoffer / Yang, Hu

    Advanced drug delivery reviews

    2011  Band 64, Heft 7, Seite(n) 605–613

    Abstract: Research into the diagnosis and treatment of central nervous system (CNS) diseases has been enhanced by rapid advances in nanotechnology and an expansion in the library of nanostructured carriers. This review discusses the latest applications of ... ...

    Abstract Research into the diagnosis and treatment of central nervous system (CNS) diseases has been enhanced by rapid advances in nanotechnology and an expansion in the library of nanostructured carriers. This review discusses the latest applications of nanomaterials in the CNS with an emphasis on brain tumors. Novel administration routes and transport mechanisms for nanomaterial-mediated CNS delivery of diagnostic and therapeutic agents to bypass or cross the blood brain barrier (BBB) are also discussed. These include temporary disruption of the BBB, use of impregnated polymers (polymer wafers), convection-enhanced delivery (CED), and intranasal delivery. Moreover, an in vitro BBB model capable of mimicking geometrical, cellular and rheological features of the human cerebrovasculature has been developed. This is a useful tool that can be used for screening CNS nanoparticles or therapeutics prior to in vivo and clinical investigation. A discussion of this novel model is included.
    Mesh-Begriff(e) Animals ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Central Nervous System/drug effects ; Central Nervous System/metabolism ; Central Nervous System Diseases/diagnosis ; Central Nervous System Diseases/drug therapy ; Central Nervous System Diseases/metabolism ; Diagnostic Uses of Chemicals ; Drug Carriers/administration & dosage ; Drug Delivery Systems/methods ; Humans ; Nanoparticles/administration & dosage ; Pharmaceutical Preparations/administration & dosage
    Chemische Substanzen Diagnostic Uses of Chemicals ; Drug Carriers ; Pharmaceutical Preparations
    Sprache Englisch
    Erscheinungsdatum 2011-12-08
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 639113-8
    ISSN 1872-8294 ; 0169-409X
    ISSN (online) 1872-8294
    ISSN 0169-409X
    DOI 10.1016/j.addr.2011.11.014
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Orally Bioavailable and Blood-Brain Barrier-Penetrating ATM Inhibitor (AZ32) Radiosensitizes Intracranial Gliomas in Mice.

    Karlin, Jeremy / Allen, Jasmine / Ahmad, Syed F / Hughes, Gareth / Sheridan, Victoria / Odedra, Rajesh / Farrington, Paul / Cadogan, Elaine B / Riches, Lucy C / Garcia-Trinidad, Antonio / Thomason, Andrew G / Patel, Bhavika / Vincent, Jennifer / Lau, Alan / Pike, Kurt G / Hunt, Thomas A / Sule, Amrita / Valerie, Nicholas C K / Biddlestone-Thorpe, Laura /
    Kahn, Jenna / Beckta, Jason M / Mukhopadhyay, Nitai / Barlaam, Bernard / Degorce, Sebastien L / Kettle, Jason / Colclough, Nicola / Wilson, Joanne / Smith, Aaron / Barrett, Ian P / Zheng, Li / Zhang, Tianwei / Wang, Yingchun / Chen, Kan / Pass, Martin / Durant, Stephen T / Valerie, Kristoffer

    Molecular cancer therapeutics

    2018  Band 17, Heft 8, Seite(n) 1637–1647

    Abstract: Inhibition of ataxia-telangiectasia mutated (ATM) during radiotherapy of glioblastoma multiforme (GBM) may improve tumor control by short-circuiting the response to radiation-induced DNA damage. A major impediment for clinical implementation is that ... ...

    Abstract Inhibition of ataxia-telangiectasia mutated (ATM) during radiotherapy of glioblastoma multiforme (GBM) may improve tumor control by short-circuiting the response to radiation-induced DNA damage. A major impediment for clinical implementation is that current inhibitors have limited central nervous system (CNS) bioavailability; thus, the goal was to identify ATM inhibitors (ATMi) with improved CNS penetration. Drug screens and refinement of lead compounds identified AZ31 and AZ32. The compounds were then tested
    Mesh-Begriff(e) Administration, Oral ; Animals ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Blood-Brain Barrier/metabolism ; Cell Line, Tumor ; Glioma/drug therapy ; Humans ; Mice ; Mice, Nude ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Radiation-Sensitizing Agents/pharmacology ; Radiation-Sensitizing Agents/therapeutic use
    Chemische Substanzen Protein Kinase Inhibitors ; Radiation-Sensitizing Agents ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2018-05-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-17-0975
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: ATM kinase inhibition preferentially sensitizes p53-mutant glioma to ionizing radiation.

    Biddlestone-Thorpe, Laura / Sajjad, Muhammad / Rosenberg, Elizabeth / Beckta, Jason M / Valerie, Nicholas C K / Tokarz, Mary / Adams, Bret R / Wagner, Alison F / Khalil, Ashraf / Gilfor, Donna / Golding, Sarah E / Deb, Sumitra / Temesi, David G / Lau, Alan / O'Connor, Mark J / Choe, Kevin S / Parada, Luis F / Lim, Sang Kyun / Mukhopadhyay, Nitai D /
    Valerie, Kristoffer

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2013  Band 19, Heft 12, Seite(n) 3189–3200

    Abstract: Purpose: Glioblastoma multiforme (GBM) is the most lethal form of brain cancer with a median survival of only 12 to 15 months. Current standard treatment consists of surgery followed by chemoradiation. The poor survival of patients with GBM is due to ... ...

    Abstract Purpose: Glioblastoma multiforme (GBM) is the most lethal form of brain cancer with a median survival of only 12 to 15 months. Current standard treatment consists of surgery followed by chemoradiation. The poor survival of patients with GBM is due to aggressive tumor invasiveness, an inability to remove all tumor tissue, and an innate tumor chemo- and radioresistance. Ataxia-telangiectasia mutated (ATM) is an excellent target for radiosensitizing GBM because of its critical role in regulating the DNA damage response and p53, among other cellular processes. As a first step toward this goal, we recently showed that the novel ATM kinase inhibitor KU-60019 reduced migration, invasion, and growth, and potently radiosensitized human glioma cells in vitro.
    Experimental design: Using orthotopic xenograft models of GBM, we now show that KU-60019 is also an effective radiosensitizer in vivo. Human glioma cells expressing reporter genes for monitoring tumor growth and dispersal were grown intracranially, and KU-60019 was administered intratumorally by convection-enhanced delivery or osmotic pump.
    Results: Our results show that the combined effect of KU-60019 and radiation significantly increased survival of mice 2- to 3-fold over controls. Importantly, we show that glioma with mutant p53 is much more sensitive to KU-60019 radiosensitization than genetically matched wild-type glioma.
    Conclusions: Taken together, our results suggest that an ATM kinase inhibitor may be an effective radiosensitizer and adjuvant therapy for patients with mutant p53 brain cancers.
    Mesh-Begriff(e) Animals ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Ataxia Telangiectasia Mutated Proteins/genetics ; Brain Neoplasms/pathology ; Brain Neoplasms/therapy ; Cell Line, Tumor ; Flow Cytometry ; Gene Expression Regulation, Neoplastic/drug effects ; Glioma/pathology ; Glioma/therapy ; Humans ; Mice ; Morpholines/administration & dosage ; Mutation ; Radiation Tolerance/drug effects ; Radiation, Ionizing ; Thioxanthenes/administration & dosage ; Tumor Suppressor Protein p53/genetics
    Chemische Substanzen 2-(2,6-dimethylmorpholin-4-yl)-N-(5-(6-morpholin-4-yl-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide ; Morpholines ; TP53 protein, human ; Thioxanthenes ; Tumor Suppressor Protein p53 ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2013-04-25
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-12-3408
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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