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  1. AU="Storey, Claire M"
  2. AU="Schwartzenburg, Joshua"
  3. AU=Charoenlap Suvanee
  4. AU="Gomez Cifuentes, Juan D" AU="Gomez Cifuentes, Juan D"
  5. AU="Marozas, J A"
  6. AU="Casimiro De Luca"
  7. AU="Julie Clarke"
  8. AU=Wybraniec Maciej T.
  9. AU="Meuwese, Christiaan L"
  10. AU="Al-Hattab, Eyad S"
  11. AU="Eduardo Díaz Cano"
  12. AU=Nrxe Dorte Schou AU=Nrxe Dorte Schou
  13. AU="Kende, Anna"
  14. AU="Nattmann, Phillip"
  15. AU="Assefa, Samuel"
  16. AU="McMahon, Teagan"
  17. AU="Radojičić Zoran"
  18. AU="Muwu Xu"
  19. AU="Sacchi, Diana"
  20. AU="Romain Berraud-Pache"
  21. AU=Johnson Paul D R
  22. AU="Sarigül-Yildirim, Figen"
  23. AU=Chang Yu-Ting
  24. AU="Xu, Ivana"
  25. AU="Linde, Lauren"
  26. AU="Brewer, Katlyn K"
  27. AU="Prow, Natalie A"
  28. AU=Venkatesan Arun
  29. AU="Russcher, H."
  30. AU="Chambino, Beatriz"
  31. AU="L'Abbé, Ericka N."
  32. AU=Moore Stephen M.
  33. AU="Gabriel, Berteșteanu Șerban Vifor" AU="Gabriel, Berteșteanu Șerban Vifor"
  34. AU="Gallo, Eduado"
  35. AU="Yurchenko, Maria"
  36. AU="Fabiana Giber"
  37. AU="Rajakumar, Gopal Suseela" AU="Rajakumar, Gopal Suseela"
  38. AU="Gutierrez, M. N"
  39. AU=Zhuo Jia L.
  40. AU=Miller Mark A
  41. AU="Dąbrowski, Leszek"
  42. AU="Röltgen, Katharina"
  43. AU="Tumanov, Alexey"
  44. AU="Berns, Lauren"
  45. AU="Elena A. Deshevaya"
  46. AU=Zhang Ruijuan
  47. AU="Mueller, Luke"
  48. AU=Barzon Luisa
  49. AU="Karunakaran, Denuja"
  50. AU="Figueroa-Rivera, Ivonne M"
  51. AU="Blackburn, Fran"
  52. AU="Lee, Hee-Kyung"
  53. AU=Kinoshita J H
  54. AU="Hernesniemi, Juha"
  55. AU="Evans, Matthew L"
  56. AU=Payne Thomas
  57. AU="Brown, Dexter"

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  1. Artikel ; Online: Quantitative In Vivo Imaging of the Androgen Receptor Axis Reveals Degree of Prostate Cancer Radiotherapy Response.

    Storey, Claire M / Altai, Mohamed / Bicak, Mesude / Veach, Darren R / Lückerath, Katharina / Adrian, Gabriel / McDevitt, Michael R / Kalidindi, Teja / Park, Julie E / Herrmann, Ken / Abou, Diane / Zedan, Wahed / Peekhaus, Norbert / Klein, Robert J / Damoiseaux, Robert / Larson, Steven M / Lilja, Hans / Thorek, Daniel / Ulmert, David

    Molecular cancer research : MCR

    2024  Band 21, Heft 4, Seite(n) 307–315

    Abstract: Noninvasive biomarkers for androgen receptor (AR) pathway activation are urgently needed to better monitor patient response to prostate cancer therapies. AR is a critical driver and mediator of resistance of prostate cancer but currently available ... ...

    Abstract Noninvasive biomarkers for androgen receptor (AR) pathway activation are urgently needed to better monitor patient response to prostate cancer therapies. AR is a critical driver and mediator of resistance of prostate cancer but currently available noninvasive prostate cancer biomarkers to monitor AR activity are discordant with downstream AR pathway activity. External beam radiotherapy (EBRT) remains a common treatment for all stages of prostate cancer, and DNA damage induced by EBRT upregulates AR pathway activity to promote therapeutic resistance. [89Zr]11B6-PET is a novel modality targeting prostate-specific protein human kallikrein 2 (hK2), which is a surrogate biomarker for AR activity. Here, we studied whether [89Zr]11B6-PET can accurately assess EBRT-induced AR activity.Genetic and human prostate cancer mouse models received EBRT (2-50 Gy) and treatment response was monitored by [89Zr]11B6-PET/CT. Radiotracer uptake and expression of AR and AR target genes was quantified in resected tissue.EBRT increased AR pathway activity and [89Zr]11B6 uptake in LNCaP-AR and 22RV1 tumors. EBRT increased prostate-specific [89Zr]11B6 uptake in prostate cancer-bearing mice (Hi-Myc x Pb_KLK2) with no significant changes in uptake in healthy (Pb_KLK2) mice, and this correlated with hK2 protein levels.
    Implications: hK2 expression in prostate cancer tissue is a proxy of EBRT-induced AR activity that can noninvasively be detected using [89Zr]11B6-PET; further clinical evaluation of hK2-PET for monitoring response and development of resistance to EBRT in real time is warranted.
    Mesh-Begriff(e) Animals ; Humans ; Male ; Mice ; Cell Line, Tumor ; Positron Emission Tomography Computed Tomography ; Prostatic Neoplasms/diagnostic imaging ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/radiotherapy ; Radioisotopes ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Zirconium
    Chemische Substanzen Radioisotopes ; Receptors, Androgen ; Zirconium (C6V6S92N3C) ; Zirconium-89 (NTM296JU95)
    Sprache Englisch
    Erscheinungsdatum 2024-03-19
    Erscheinungsland United States
    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.
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-22-0736
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: SDHB knockout and succinate accumulation are insufficient for tumorigenesis but dual SDHB/NF1 loss yields SDHx-like pheochromocytomas.

    Armstrong, Neali / Storey, Claire M / Noll, Sarah E / Margulis, Katherine / Soe, Myat Han / Xu, Haixia / Yeh, Benjamin / Fishbein, Lauren / Kebebew, Electron / Howitt, Brooke E / Zare, Richard N / Sage, Julien / Annes, Justin P

    Cell reports

    2022  Band 38, Heft 9, Seite(n) 110453

    Abstract: Inherited pathogenic succinate dehydrogenase (SDHx) gene mutations cause the hereditary pheochromocytoma and paraganglioma tumor syndrome. Syndromic tumors exhibit elevated succinate, an oncometabolite that is proposed to drive tumorigenesis via DNA and ... ...

    Abstract Inherited pathogenic succinate dehydrogenase (SDHx) gene mutations cause the hereditary pheochromocytoma and paraganglioma tumor syndrome. Syndromic tumors exhibit elevated succinate, an oncometabolite that is proposed to drive tumorigenesis via DNA and histone hypermethylation, mitochondrial expansion, and pseudohypoxia-related gene expression. To interrogate this prevailing model, we disrupt mouse adrenal medulla SDHB expression, which recapitulates several key molecular features of human SDHx tumors, including succinate accumulation but not 5hmC loss, HIF accumulation, or tumorigenesis. By contrast, concomitant SDHB and the neurofibromin 1 tumor suppressor disruption yields SDHx-like pheochromocytomas. Unexpectedly, in vivo depletion of the 2-oxoglutarate (2-OG) dioxygenase cofactor ascorbate reduces SDHB-deficient cell survival, indicating that SDHx loss may be better tolerated by tissues with high antioxidant capacity. Contrary to the prevailing oncometabolite model, succinate accumulation and 2-OG-dependent dioxygenase inhibition are insufficient for mouse pheochromocytoma tumorigenesis, which requires additional growth-regulatory pathway activation.
    Mesh-Begriff(e) Adrenal Gland Neoplasms/genetics ; Adrenal Gland Neoplasms/metabolism ; Adrenal Gland Neoplasms/pathology ; Animals ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic ; Dioxygenases/metabolism ; Mice ; Pheochromocytoma/genetics ; Pheochromocytoma/metabolism ; Pheochromocytoma/pathology ; Succinate Dehydrogenase/genetics ; Succinate Dehydrogenase/metabolism ; Succinates ; Succinic Acid/metabolism
    Chemische Substanzen Succinates ; Succinic Acid (AB6MNQ6J6L) ; Dioxygenases (EC 1.13.11.-) ; Succinate Dehydrogenase (EC 1.3.99.1)
    Sprache Englisch
    Erscheinungsdatum 2022-03-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110453
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Mapping the Structural Determinants Required for AAVrh.10 Transport across the Blood-Brain Barrier.

    Albright, Blake H / Storey, Claire M / Murlidharan, Giridhar / Castellanos Rivera, Ruth M / Berry, Garrett E / Madigan, Victoria J / Asokan, Aravind

    Molecular therapy : the journal of the American Society of Gene Therapy

    2017  Band 26, Heft 2, Seite(n) 510–523

    Abstract: Effective gene delivery to the CNS by intravenously administered adeno-associated virus (AAV) vectors requires crossing the blood-brain barrier (BBB). To achieve therapeutic CNS transgene expression, high systemic vector doses are often required, which ... ...

    Abstract Effective gene delivery to the CNS by intravenously administered adeno-associated virus (AAV) vectors requires crossing the blood-brain barrier (BBB). To achieve therapeutic CNS transgene expression, high systemic vector doses are often required, which poses challenges such as scale-up costs and dose-dependent hepatotoxicity. To improve the specificity and efficiency of CNS gene transfer, a better understanding of the structural features that enable AAV transit across the BBB is needed. We generated a combinatorial domain swap library using AAV1, a serotype that does not traverse the vasculature, and AAVrh.10, which crosses the BBB in mice. We then screened individual variants by phylogenetic and structural analyses and subsequently conducted systemic characterization in mice. Using this approach, we identified key clusters of residues on the AAVrh.10 capsid that enabled transport across the brain vasculature and widespread neuronal transduction in mice. Through rational design, we mapped a minimal footprint from AAVrh.10, which, when grafted onto AAV1, confers the aforementioned CNS phenotype while diminishing vascular and hepatic transduction through an unknown mechanism. Functional mapping of this capsid surface footprint provides a roadmap for engineering synthetic AAV capsids for efficient CNS gene transfer with an improved safety profile.
    Mesh-Begriff(e) Animals ; Biological Transport ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/virology ; Brain/metabolism ; Capsid Proteins/chemistry ; Capsid Proteins/genetics ; Dependovirus/classification ; Dependovirus/physiology ; Dependovirus/ultrastructure ; Gene Expression ; Gene Transfer Techniques ; Genetic Engineering ; Genetic Vectors/administration & dosage ; Humans ; Mice ; Models, Molecular ; Myocardium/metabolism ; Organ Specificity ; Phylogeny ; Protein Binding ; Tissue Distribution ; Transduction, Genetic ; Transgenes
    Chemische Substanzen Capsid Proteins
    Sprache Englisch
    Erscheinungsdatum 2017-10-26
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2010592-7
    ISSN 1525-0024 ; 1525-0016
    ISSN (online) 1525-0024
    ISSN 1525-0016
    DOI 10.1016/j.ymthe.2017.10.017
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: PSA-Targeted Alpha-, Beta-, and Positron-Emitting Immunotheranostics in Murine Prostate Cancer Models and Nonhuman Primates.

    Veach, Darren R / Storey, Claire M / Lückerath, Katharina / Braun, Katharina / von Bodman, Christian / Lamminmäki, Urpo / Kalidindi, Teja / Strand, Sven-Erik / Strand, Joanna / Altai, Mohamed / Damoiseaux, Robert / Zanzonico, Pat / Benabdallah, Nadia / Pankov, Dmitry / Scher, Howard I / Scardino, Peter / Larson, Steven M / Lilja, Hans / McDevitt, Michael R /
    Thorek, Daniel L J / Ulmert, David

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

    2021  Band 27, Heft 7, Seite(n) 2050–2060

    Abstract: Purpose: Most patients with prostate cancer treated with androgen receptor (AR) signaling inhibitors develop therapeutic resistance due to restoration of AR functionality. Thus, there is a critical need for novel treatment approaches. Here we ... ...

    Abstract Purpose: Most patients with prostate cancer treated with androgen receptor (AR) signaling inhibitors develop therapeutic resistance due to restoration of AR functionality. Thus, there is a critical need for novel treatment approaches. Here we investigate the theranostic potential of hu5A10, a humanized mAb specifically targeting free PSA (
    Experimental design: LNCaP-AR (LNCaP with overexpression of wildtype AR) xenografts (NSG mice) and
    Results: Biodistribution of radiolabeled hu5A10 constructs was comparable in different mouse models. Specific tumor uptake increased over time and correlated with PSA expression. Treatment with [
    Conclusions: We present a complete preclinical evaluation of radiolabeled hu5A10 in mouse prostate cancer models and NHPs, and establish hu5A10 as a new theranostic agent that allows highly specific and effective downstream targeting of AR in PSA-expressing tissue. Our data support the clinical translation of radiolabeled hu5A10 for treating prostate cancer.
    Mesh-Begriff(e) Alpha Particles/therapeutic use ; Animals ; Beta Particles/therapeutic use ; Disease Models, Animal ; Electrons/therapeutic use ; Linear Energy Transfer ; Macaca fascicularis ; Male ; Mice ; Mice, Inbred BALB C ; Positron-Emission Tomography ; Prostate-Specific Antigen/immunology ; Prostate-Specific Antigen/metabolism ; Prostatic Neoplasms/radiotherapy ; Radioimmunotherapy/methods ; Receptors, Androgen/physiology ; Tissue Distribution
    Chemische Substanzen Receptors, Androgen ; Prostate-Specific Antigen (EC 3.4.21.77)
    Sprache Englisch
    Erscheinungsdatum 2021-01-13
    Erscheinungsland United States
    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.
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-20-3614
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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