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  1. AU="Hrvoje Miletic"
  2. AU="Hardick, Justin"
  3. AU="Peiris, Alan N"
  4. AU="Lei Ke"
  5. AU="Mian-Hua Cai"
  6. AU=Lanzerath Dirk
  7. AU=Cakir Murat
  8. AU="Ng, Frank"
  9. AU="Miley, D"
  10. AU=Dikken Dirk Jan W.
  11. AU="Nasehi, Nahal"
  12. AU="Arun Seth"
  13. AU="Woitok, Mira"
  14. AU="Amparo MoraguesauthorDpto. Ingeniera Civil: Construccin, E.T.S.I. de Caminos, Canales y Puertos, Universidad Politcnica de Madrid, C/ Profesor Aranguren 3, 28040 Madrid, Spain"
  15. AU="Guidry, Jessie"
  16. AU=Mitry Maria A.
  17. AU="Rhodes, Rosamond"
  18. AU="Gromova, Alexandra S"
  19. AU=Ockene Ira
  20. AU=Hirsch Daniela
  21. AU=Navaratnam Annalan MD
  22. AU="Johnson, Matthew Thomas"
  23. AU=Wagstaff Peter GK
  24. AU="Almahboub, Sarah A"
  25. AU="Tuana Aksu"
  26. AU="Bozin, Tonci"
  27. AU="Rachel Marie Towle"
  28. AU="Soriano-Ursúa, Marvin A"
  29. AU="Cagnin, A"
  30. AU="Ivens, Al C"
  31. AU="Juan Mucci"
  32. AU="Alejandro Hlavnika"
  33. AU="Makarenko V."

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  1. Article ; Online: Therapeutic implications of altered cholesterol homeostasis mediated by loss of CYP46A1 in human glioblastoma

    Mingzhi Han / Shuai Wang / Ning Yang / Xu Wang / Wenbo Zhao / Halala Sdik Saed / Thomas Daubon / Bin Huang / Anjing Chen / Gang Li / Hrvoje Miletic / Frits Thorsen / Rolf Bjerkvig / Xingang Li / Jian Wang

    EMBO Molecular Medicine, Vol 12, Iss 1, Pp n/a-n/a (2020)

    2020  

    Abstract: Abstract Dysregulated cholesterol metabolism is a hallmark of many cancers, including glioblastoma (GBM), but its role in disease progression is not well understood. Here, we identified cholesterol 24‐hydroxylase (CYP46A1), a brain‐specific enzyme ... ...

    Abstract Abstract Dysregulated cholesterol metabolism is a hallmark of many cancers, including glioblastoma (GBM), but its role in disease progression is not well understood. Here, we identified cholesterol 24‐hydroxylase (CYP46A1), a brain‐specific enzyme responsible for the elimination of cholesterol through the conversion of cholesterol into 24(S)‐hydroxycholesterol (24OHC), as one of the most dramatically dysregulated cholesterol metabolism genes in GBM. CYP46A1 was significantly decreased in GBM samples compared with normal brain tissue. A reduction in CYP46A1 expression was associated with increasing tumour grade and poor prognosis in human gliomas. Ectopic expression of CYP46A1 suppressed cell proliferation and in vivo tumour growth by increasing 24OHC levels. RNA‐seq revealed that treatment of GBM cells with 24OHC suppressed tumour growth through regulation of LXR and SREBP signalling. Efavirenz, an activator of CYP46A1 that is known to penetrate the blood–brain barrier, inhibited GBM growth in vivo. Our findings demonstrate that CYP46A1 is a critical regulator of cellular cholesterol in GBM and that the CYP46A1/24OHC axis is a potential therapeutic target.
    Keywords 24OHC ; cholesterol homeostasis ; CYP46A1 ; efavirenz ; glioblastoma ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Subject code 616
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Oncolytic H-1 parvovirus binds to sialic acid on laminins for cell attachment and entry

    Amit Kulkarni / Tiago Ferreira / Clemens Bretscher / Annabel Grewenig / Nazim El-Andaloussi / Serena Bonifati / Tiina Marttila / Valérie Palissot / Jubayer A. Hossain / Francisco Azuaje / Hrvoje Miletic / Lars A. R. Ystaas / Anna Golebiewska / Simone P. Niclou / Ralf Roeth / Beate Niesler / Amélie Weiss / Laurent Brino / Antonio Marchini

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Volume 18

    Abstract: Rat H-1 parvovirus (H-1PV) is in clinical development for oncolytic therapy. Here, Kulkarni et al. identify LAMC1 as a modulator of H-1PV cell attachment and entry and find that LAMC1 levels and H-1PV oncolytic activity correlate in 59 tested cancer cell ...

    Abstract Rat H-1 parvovirus (H-1PV) is in clinical development for oncolytic therapy. Here, Kulkarni et al. identify LAMC1 as a modulator of H-1PV cell attachment and entry and find that LAMC1 levels and H-1PV oncolytic activity correlate in 59 tested cancer cell lines.
    Keywords Science ; Q
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Lactate dehydrogenases promote glioblastoma growth and invasion via a metabolic symbiosis

    Joris Guyon / Ignacio Fernandez‐Moncada / Claire M Larrieu / Cyrielle L Bouchez / Antonio C Pagano Zottola / Johanna Galvis / Tiffanie Chouleur / Audrey Burban / Kevin Joseph / Vidhya M Ravi / Heidi Espedal / Gro Vatne Røsland / Boutaina Daher / Aurélien Barre / Benjamin Dartigues / Slim Karkar / Justine Rudewicz / Irati Romero‐Garmendia / Barbara Klink /
    Konrad Grützmann / Marie‐Alix Derieppe / Thibaut Molinié / Nina Obad / Céline Léon / Giorgio Seano / Hrvoje Miletic / Dieter Henrik Heiland / Giovanni Marsicano / Macha Nikolski / Rolf Bjerkvig / Andreas Bikfalvi / Thomas Daubon

    EMBO Molecular Medicine, Vol 14, Iss 12, Pp n/a-n/a (2022)

    2022  

    Abstract: Abstract Lactate is a central metabolite in brain physiology but also contributes to tumor development. Glioblastoma (GB) is the most common and malignant primary brain tumor in adults, recognized by angiogenic and invasive growth, in addition to its ... ...

    Abstract Abstract Lactate is a central metabolite in brain physiology but also contributes to tumor development. Glioblastoma (GB) is the most common and malignant primary brain tumor in adults, recognized by angiogenic and invasive growth, in addition to its altered metabolism. We show herein that lactate fuels GB anaplerosis by replenishing the tricarboxylic acid (TCA) cycle in absence of glucose. Lactate dehydrogenases (LDHA and LDHB), which we found spatially expressed in GB tissues, catalyze the interconversion of pyruvate and lactate. However, ablation of both LDH isoforms, but not only one, led to a reduction in tumor growth and an increase in mouse survival. Comparative transcriptomics and metabolomics revealed metabolic rewiring involving high oxidative phosphorylation (OXPHOS) in the LDHA/B KO group which sensitized tumors to cranial irradiation, thus improving mouse survival. When mice were treated with the antiepileptic drug stiripentol, which targets LDH activity, tumor growth decreased. Our findings unveil the complex metabolic network in which both LDHA and LDHB are integrated and show that the combined inhibition of LDHA and LDHB strongly sensitizes GB to therapy.
    Keywords antiepileptic drug ; energy metabolism ; glioblastoma ; invasion ; lactate dehydrogenases ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Subject code 570
    Language English
    Publishing date 2022-12-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Correction

    Peter C Huszthy / Per Ø Sakariassen / Heidi Espedal / Karl A Brokstad / Rolf Bjerkvig / Hrvoje Miletic

    PLoS ONE, Vol 10, Iss 10, p e

    Engraftment of Human Glioblastoma Cells in Immunocompetent Rats through Acquired Immunosuppression.

    2015  Volume 0140303

    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Engraftment of Human Glioblastoma Cells in Immunocompetent Rats through Acquired Immunosuppression.

    Peter C Huszthy / Per Ø Sakariassen / Heidi Espedal / Karl A Brokstad / Rolf Bjerkvig / Hrvoje Miletic

    PLoS ONE, Vol 10, Iss 8, p e

    2015  Volume 0136089

    Abstract: Transplantation of glioblastoma patient biopsy spheroids to the brain of T cell-compromised Rowett (nude) rats has been established as a representative animal model for human GBMs, with a tumor take rate close to 100%. In immunocompetent littermates ... ...

    Abstract Transplantation of glioblastoma patient biopsy spheroids to the brain of T cell-compromised Rowett (nude) rats has been established as a representative animal model for human GBMs, with a tumor take rate close to 100%. In immunocompetent littermates however, primary human GBM tissue is invariably rejected. Here we show that after repeated passaging cycles in nude rats, human GBM spheroids are enabled to grow in the brain of immunocompetent rats. In case of engraftment, xenografts in immunocompetent rats grow progressively and host leukocytes fail to enter the tumor bed, similar to what is seen in nude animals. In contrast, rejection is associated with massive infiltration of the tumor bed by leukocytes, predominantly ED1+ microglia/macrophages, CD4+ T helper cells and CD8+ effector cells, and correlates with elevated serum levels of pro-inflammatory cytokines IL-1α, IL-18 and TNF-α [corrected]. We observed that in nude rat brains, an adaptation to the host occurs after several in vivo passaging cycles, characterized by striking attenuation of microglial infiltration. Furthermore, tumor-derived chemokines that promote leukocyte migration and their entry into the CNS such as CXCL-10 and CXCL-12 are down-regulated, and the levels of TGF-β2 increase. We propose that through serial in vivo passaging in nude rats, human GBM cells learn to avoid and or/ suppress host immunity. Such adapted GBM cells are in turn able to engraft in immunocompetent rats without signs of an inflammatory response.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Deciphering the complex role of thrombospondin-1 in glioblastoma development

    Thomas Daubon / Céline Léon / Kim Clarke / Laetitia Andrique / Laura Salabert / Elodie Darbo / Raphael Pineau / Sylvaine Guérit / Marlène Maitre / Stéphane Dedieu / Albin Jeanne / Sabine Bailly / Jean-Jacques Feige / Hrvoje Miletic / Marco Rossi / Lorenzo Bello / Francesco Falciani / Rolf Bjerkvig / Andréas Bikfalvi

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 15

    Abstract: Thrombospondin-1 (THSB1) is a component of the ECM with a role in regulating cancer development and tumour vasculature. Here, the authors show that TGF-beta-induced THBS1 expression contributes to the invasive behaviour of GBM cells and promotes ... ...

    Abstract Thrombospondin-1 (THSB1) is a component of the ECM with a role in regulating cancer development and tumour vasculature. Here, the authors show that TGF-beta-induced THBS1 expression contributes to the invasive behaviour of GBM cells and promotes resistance to antiangiogenic therapy partially through interaction with CD47.
    Keywords Science ; Q
    Language English
    Publishing date 2019-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Deciphering the complex role of thrombospondin-1 in glioblastoma development

    Thomas Daubon / Céline Léon / Kim Clarke / Laetitia Andrique / Laura Salabert / Elodie Darbo / Raphael Pineau / Sylvaine Guérit / Marlène Maitre / Stéphane Dedieu / Albin Jeanne / Sabine Bailly / Jean-Jacques Feige / Hrvoje Miletic / Marco Rossi / Lorenzo Bello / Francesco Falciani / Rolf Bjerkvig / Andréas Bikfalvi

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 15

    Abstract: Thrombospondin-1 (THSB1) is a component of the ECM with a role in regulating cancer development and tumour vasculature. Here, the authors show that TGF-beta-induced THBS1 expression contributes to the invasive behaviour of GBM cells and promotes ... ...

    Abstract Thrombospondin-1 (THSB1) is a component of the ECM with a role in regulating cancer development and tumour vasculature. Here, the authors show that TGF-beta-induced THBS1 expression contributes to the invasive behaviour of GBM cells and promotes resistance to antiangiogenic therapy partially through interaction with CD47.
    Keywords Science ; Q
    Language English
    Publishing date 2019-03-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Microglia Induce PDGFRB Expression in Glioma Cells to Enhance Their Migratory Capacity

    Tatjana Wallmann / Xing-Mei Zhang / Majken Wallerius / Sara Bolin / Anne-Laure Joly / Caroline Sobocki / Lina Leiss / Yiwen Jiang / Jonas Bergh / Eric C. Holland / Per Ø. Enger / John Andersson / Fredrik J. Swartling / Hrvoje Miletic / Lene Uhrbom / Robert A. Harris / Charlotte Rolny

    iScience, Vol 9, Iss , Pp 71-

    2018  Volume 83

    Abstract: Summary: High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established ... ...

    Abstract Summary: High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. : Pathophysiology; Molecular Mechanism of Behavior; Immunology; Cancer Subject Areas: Pathophysiology, Molecular Mechanism of Behavior, Immunology, Cancer
    Keywords Science ; Q
    Subject code 616
    Language English
    Publishing date 2018-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Correction

    Jorge A. Benitez / Jianhui Ma / Matteo D’Antonio / Antonia Boyer / Maria Fernanda Camargo / Ciro Zanca / Stephen Kelly / Alireza Khodadadi-Jamayran / Nathan M. Jameson / Michael Andersen / Hrvoje Miletic / Shahram Saberi / Kelly A. Frazer / Webster K. Cavenee / Frank B. Furnari

    Nature Communications, Vol 9, Iss 1, Pp 1-

    Publisher Correction: PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3

    2018  Volume 1

    Abstract: Nature Communications 8:15223 doi: (2017); Published 12 May 2017; Updated 25 May 2018 The originally published version of this Article contained an error in Fig. 1. In panel d, the uppermost western blot was inadvertently inverted during typesetting of ... ...

    Abstract Nature Communications 8:15223 doi: (2017); Published 12 May 2017; Updated 25 May 2018 The originally published version of this Article contained an error in Fig. 1. In panel d, the uppermost western blot was inadvertently inverted during typesetting of the figure. This has now been corrected in boththe PDF and HTML versions of the Article.
    Keywords Science ; Q
    Language English
    Publishing date 2018-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Novel SLC19A3 Promoter Deletion and Allelic Silencing in Biotin-Thiamine-Responsive Basal Ganglia Encephalopathy.

    Irene Flønes / Paweł Sztromwasser / Kristoffer Haugarvoll / Christian Dölle / Maria Lykouri / Thomas Schwarzlmüller / Inge Jonassen / Hrvoje Miletic / Stefan Johansson / Per M Knappskog / Laurence A Bindoff / Charalampos Tzoulis

    PLoS ONE, Vol 11, Iss 2, p e

    2016  Volume 0149055

    Abstract: BACKGROUND:Biotin-thiamine responsive basal ganglia disease is a severe, but potentially treatable disorder caused by mutations in the SLC19A3 gene. Although the disease is inherited in an autosomal recessive manner, patients with typical phenotypes ... ...

    Abstract BACKGROUND:Biotin-thiamine responsive basal ganglia disease is a severe, but potentially treatable disorder caused by mutations in the SLC19A3 gene. Although the disease is inherited in an autosomal recessive manner, patients with typical phenotypes carrying single heterozygous mutations have been reported. This makes the diagnosis uncertain and may delay treatment. METHODS AND RESULTS:In two siblings with early-onset encephalopathy dystonia and epilepsy, whole-exome sequencing revealed a novel single heterozygous SLC19A3 mutation (c.337T>C). Although Sanger-sequencing and copy-number analysis revealed no other aberrations, RNA-sequencing in brain tissue suggested the second allele was silenced. Whole-genome sequencing resolved the genetic defect by revealing a novel 45,049 bp deletion in the 5'-UTR region of the gene abolishing the promoter. High dose thiamine and biotin therapy was started in the surviving sibling who remains stable. In another patient two novel compound heterozygous SLC19A3 mutations were found. He improved substantially on thiamine and biotin therapy. CONCLUSIONS:We show that large genomic deletions occur in the regulatory region of SLC19A3 and should be considered in genetic testing. Moreover, our study highlights the power of whole-genome sequencing as a diagnostic tool for rare genetic disorders across a wide spectrum of mutations including non-coding large genomic rearrangements.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616 ; 572
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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