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  1. AU="Laemmerer, Anna"
  2. AU="Guedes, Tássia T A M"
  3. AU=Savoie L L
  4. AU="Huang, Tsai-Wei"
  5. AU="Michael Pugliese"
  6. AU="Amador-Sánchez, Yoarhy A"
  7. AU="Lanbo Shi"
  8. AU="Gregg, R J"
  9. AU="Zou, Peiyuan"
  10. AU="Sasha Stevenson"
  11. AU="Boncompagni, Alessandra"
  12. AU="Lewis, Annisa L"
  13. AU="Daniel Freilich"
  14. AU="Glascock, Abigail L"
  15. AU="Gordon Bernard"
  16. AU="Lv, Mengwen"
  17. AU="Rottman Pietrzak, Kathleen A"
  18. AU=Panczak Radoslaw
  19. AU="Hosseini, Seyed Mohammad Hadi"
  20. AU="Noda, Haruna"
  21. AU="Raoul, Cédric"
  22. AU=Wissing Silke AU=Wissing Silke
  23. AU="Chun-Lin Yang"
  24. AU="Romine, Kyle A"
  25. AU="Cunsolo, Vincenzo"
  26. AU="Ba, Aboubacar"
  27. AU="Prisca, Mirandolina"
  28. AU="Perez, Tate"
  29. AU="Bakkaloglu, Sevan"
  30. AU="Guernieri, Rebecca L"
  31. AU="Xing, Z Y"
  32. AU="Yu-Heng Cheng"
  33. AU=Freeman Richard B Jr
  34. AU="Wang, Qi-En"
  35. AU="Mallamaci, M"
  36. AU="Turk, Yael R"
  37. AU="Tinto, Monica"
  38. AU="Selvendiran, Karuppaiyah" AU="Selvendiran, Karuppaiyah"
  39. AU="Enns, Murray W"
  40. AU="Yaohua Yang" AU="Yaohua Yang"

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  1. Artikel: Development of a cobalt(iii)-based ponatinib prodrug system.

    Mathuber, Marlene / Gutmann, Michael / La Franca, Mery / Vician, Petra / Laemmerer, Anna / Moser, Patrick / Keppler, Bernhard K / Berger, Walter / Kowol, Christian R

    Inorganic chemistry frontiers

    2021  Band 8, Heft 10, Seite(n) 2468–2485

    Abstract: Receptor tyrosine kinase inhibitors have become a central part of modern targeted cancer therapy. However, their curative potential is distinctly limited by both rapid resistance development and severe adverse effects. Consequently, tumor-specific drug ... ...

    Abstract Receptor tyrosine kinase inhibitors have become a central part of modern targeted cancer therapy. However, their curative potential is distinctly limited by both rapid resistance development and severe adverse effects. Consequently, tumor-specific drug activation based on prodrug designs, exploiting tumor-specific properties such as hypoxic oxygen conditions, is a feasible strategy to widen the therapeutic window. After proof-of-principal molecular docking studies, we have synthesized two cobalt(iii) complexes using a derivative of the clinically approved Abelson (ABL) kinase and fibroblast growth factor receptor (FGFR) inhibitor ponatinib. Acetylacetone (acac) or methylacetylacetone (Meacac) have been used as ancillary ligands to modulate the reduction potential. The ponatinib derivative, characterized by an ethylenediamine moiety instead of the piperazine ring, exhibited comparable cell-free target kinase inhibition potency. Hypoxia-dependent release of the ligand from the cobalt(iii) complexes was proven by changed fluorescence properties, enhanced downstream signaling inhibition and increased
    Sprache Englisch
    Erscheinungsdatum 2021-03-30
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 2052-1553
    ISSN 2052-1553
    DOI 10.1039/d1qi00211b
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: A whole-genome scan for Artemisinin cytotoxicity reveals a novel therapy for human brain tumors.

    Taubenschmid-Stowers, Jasmin / Orthofer, Michael / Laemmerer, Anna / Krauditsch, Christian / Rózsová, Marianna / Studer, Christian / Lötsch, Daniela / Gojo, Johannes / Gabler, Lisa / Dyczynski, Matheus / Efferth, Thomas / Hagelkruys, Astrid / Widhalm, Georg / Peyrl, Andreas / Spiegl-Kreinecker, Sabine / Hoepfner, Dominic / Bian, Shan / Berger, Walter / Knoblich, Juergen A /
    Elling, Ulrich / Horn, Moritz / Penninger, Josef M

    EMBO molecular medicine

    2023  Band 15, Heft 3, Seite(n) e16959

    Abstract: The natural compound Artemisinin is the most widely used antimalarial drug worldwide. Based on its cytotoxicity, it is also used for anticancer therapy. Artemisinin and its derivates are endoperoxides that damage proteins in eukaryotic cells; their ... ...

    Abstract The natural compound Artemisinin is the most widely used antimalarial drug worldwide. Based on its cytotoxicity, it is also used for anticancer therapy. Artemisinin and its derivates are endoperoxides that damage proteins in eukaryotic cells; their definite mechanism of action and host cell targets, however, have remained largely elusive. Using yeast and haploid stem cell screening, we demonstrate that a single cellular pathway, namely porphyrin (heme) biosynthesis, is required for the cytotoxicity of Artemisinins. Genetic or pharmacological modulation of porphyrin production is sufficient to alter its cytotoxicity in eukaryotic cells. Using multiple model systems of human brain tumor development, such as cerebral glioblastoma organoids, and patient-derived tumor spheroids, we sensitize cancer cells to dihydroartemisinin using the clinically approved porphyrin enhancer and surgical fluorescence marker 5-aminolevulinic acid, 5-ALA. A combination treatment of Artemisinins and 5-ALA markedly and specifically killed brain tumor cells in all model systems tested, including orthotopic patient-derived xenografts in vivo. These data uncover the critical molecular pathway for Artemisinin cytotoxicity and a sensitization strategy to treat different brain tumors, including drug-resistant human glioblastomas.
    Mesh-Begriff(e) Humans ; Artemisinins/pharmacology ; Artemisinins/therapeutic use ; Antimalarials/pharmacology ; Heme/metabolism ; Aminolevulinic Acid ; Brain Neoplasms/drug therapy
    Chemische Substanzen artemisinin (9RMU91N5K2) ; Artemisinins ; Antimalarials ; Heme (42VZT0U6YR) ; Aminolevulinic Acid (88755TAZ87)
    Sprache Englisch
    Erscheinungsdatum 2023-02-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202216959
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Nanoformulations of anticancer FGFR inhibitors with improved therapeutic index.

    Kallus, Sebastian / Englinger, Bernhard / Senkiv, Julia / Laemmerer, Anna / Heffeter, Petra / Berger, Walter / Kowol, Christian R / Keppler, Bernhard K

    Nanomedicine : nanotechnology, biology, and medicine

    2018  Band 14, Heft 8, Seite(n) 2632–2643

    Abstract: Fibroblast growth factor receptor (FGFR) inhibitors like ponatinib and nintedanib are clinically approved for defined cancer patient cohorts but often exert dose-limiting adverse effects. Hence, we encapsulated the FGFR inhibitors ponatinib, PD173074, ... ...

    Abstract Fibroblast growth factor receptor (FGFR) inhibitors like ponatinib and nintedanib are clinically approved for defined cancer patient cohorts but often exert dose-limiting adverse effects. Hence, we encapsulated the FGFR inhibitors ponatinib, PD173074, and nintedanib into polylactic acid nanoparticles and liposomes to enable increased tumor accumulation/specificity and reduce side effects. Different methods of drug loading were tested and the resulting formulations compared regarding average size distribution as well as encapsulation efficiency. Appropriate encapsulation levels were achieved for liposomal preparations only. Nanoencapsulation resulted in significantly decelerated uptake kinetics in vitro with clearly decreased short-term (up to 72 h) cytotoxicity at higher concentrations. However, in long-term clonogenic assays liposomal formations were equally or even more active as compared to the free drugs. Accordingly, in an FGFR inhibitor-sensitive murine osteosarcoma transplantation model (K7M2), only liposomal but not free ponatinib resulted in significant tumor growth inhibition (by 60.4%) at markedly reduced side effects.
    Mesh-Begriff(e) Animals ; Bone Neoplasms/drug therapy ; Bone Neoplasms/metabolism ; Bone Neoplasms/pathology ; Cell Proliferation/drug effects ; Enzyme Inhibitors/pharmacology ; Humans ; Imidazoles/pharmacology ; Indoles/pharmacology ; Liposomes/administration & dosage ; Liposomes/chemistry ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Nanoparticles/administration & dosage ; Nanoparticles/chemistry ; Osteosarcoma/drug therapy ; Osteosarcoma/metabolism ; Osteosarcoma/pathology ; Pyridazines/pharmacology ; Receptor, Fibroblast Growth Factor, Type 1/antagonists & inhibitors ; Therapeutic Index ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
    Chemische Substanzen Enzyme Inhibitors ; Imidazoles ; Indoles ; Liposomes ; Pyridazines ; ponatinib (4340891KFS) ; FGFR1 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1) ; nintedanib (G6HRD2P839)
    Sprache Englisch
    Erscheinungsdatum 2018-08-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2183417-9
    ISSN 1549-9642 ; 1549-9634
    ISSN (online) 1549-9642
    ISSN 1549-9634
    DOI 10.1016/j.nano.2018.08.001
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Lipid droplet-mediated scavenging as novel intrinsic and adaptive resistance factor against the multikinase inhibitor ponatinib.

    Englinger, Bernhard / Laemmerer, Anna / Moser, Patrick / Kallus, Sebastian / Röhrl, Clemens / Pirker, Christine / Baier, Dina / Mohr, Thomas / Niederstaetter, Laura / Meier-Menches, Samuel M / Gerner, Christopher / Gabler, Lisa / Gojo, Johannes / Timelthaler, Gerald / Senkiv, Julia / Jäger, Walter / Kowol, Christian R / Heffeter, Petra / Berger, Walter

    International journal of cancer

    2020  Band 147, Heft 6, Seite(n) 1680–1693

    Abstract: Ponatinib is a small molecule multi-tyrosine kinase inhibitor clinically approved for anticancer therapy. Molecular mechanisms by which cancer cells develop resistance against ponatinib are currently poorly understood. Likewise, intracellular drug ... ...

    Abstract Ponatinib is a small molecule multi-tyrosine kinase inhibitor clinically approved for anticancer therapy. Molecular mechanisms by which cancer cells develop resistance against ponatinib are currently poorly understood. Likewise, intracellular drug dynamics, as well as potential microenvironmental factors affecting the activity of this compound are unknown. Cell/molecular biological and analytical chemistry methods were applied to investigate uptake kinetics/subcellular distribution, the role of lipid droplets (LDs) and lipoid microenvironment compartments in responsiveness of FGFR1-driven lung cancer cells toward ponatinib. Selection of lung cancer cells for acquired ponatinib resistance resulted in elevated intracellular lipid levels. Uncovering intrinsic ponatinib fluorescence enabled dissection of drug uptake/retention kinetics in vitro as well as in mouse tissue cryosections, and revealed selective drug accumulation in LDs of cancer cells. Pharmacological LD upmodulation or downmodulation indicated that the extent of LD formation and consequent ponatinib incorporation negatively correlated with anticancer drug efficacy. Co-culturing with adipocytes decreased ponatinib levels and fostered survival of cancer cells. Ponatinib-selected cancer cells exhibited increased LD levels and enhanced ponatinib deposition into this organelle. Our findings demonstrate intracellular deposition of the clinically approved anticancer compound ponatinib into LDs. Furthermore, increased LD biogenesis was identified as adaptive cancer cell-defense mechanism via direct drug scavenging. Together, this suggests that LDs represent an underestimated organelle influencing intracellular pharmacokinetics and activity of anticancer tyrosine kinase inhibitors. Targeting LD integrity might constitute a strategy to enhance the activity not only of ponatinib, but also other clinically approved, lipophilic anticancer therapeutics.
    Mesh-Begriff(e) Animals ; Cell Line, Tumor ; Cell Proliferation ; Drug Resistance, Neoplasm ; Humans ; Imidazoles/pharmacokinetics ; Imidazoles/therapeutic use ; Lipid Droplets/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Protein Kinase Inhibitors/pharmacokinetics ; Protein Kinase Inhibitors/therapeutic use ; Pyridazines/pharmacokinetics ; Pyridazines/therapeutic use ; Receptor, Fibroblast Growth Factor, Type 1/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Signal Transduction ; Tumor Microenvironment ; Xenograft Model Antitumor Assays
    Chemische Substanzen Imidazoles ; Protein Kinase Inhibitors ; Pyridazines ; ponatinib (4340891KFS) ; FGFR1 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2020-03-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.32924
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 478: Hefte anzeigen Standort:
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  5. Artikel: Lysosomal Sequestration Impairs the Activity of the Preclinical FGFR Inhibitor PD173074.

    Englinger, Bernhard / Kallus, Sebastian / Senkiv, Julia / Laemmerer, Anna / Moser, Patrick / Gabler, Lisa / Groza, Diana / Kowol, Christian R / Heffeter, Petra / Grusch, Michael / Berger, Walter

    Cells

    2018  Band 7, Heft 12

    Abstract: Knowledge of intracellular pharmacokinetics of anticancer agents is imperative for understanding drug efficacy as well as intrinsic and acquired cellular resistance mechanisms. However, the factors driving subcellular drug distribution are complex and ... ...

    Abstract Knowledge of intracellular pharmacokinetics of anticancer agents is imperative for understanding drug efficacy as well as intrinsic and acquired cellular resistance mechanisms. However, the factors driving subcellular drug distribution are complex and poorly understood. Here, we describe for the first time the intrinsic fluorescence properties of the fibroblast growth factor receptor inhibitor PD1703074 as well as utilization of this physicochemical feature to investigate intracellular accumulation and compartmentalization of this compound in human lung cancer cells. Cell-free PD173074 fluorescence, intracellular accumulation and distribution were investigated using analytical chemistry and molecular biology approaches. Analyses on a subcellular scale revealed selective drug accumulation in lysosomes. Coincubation with inhibitors of lysosomal acidification strongly enhanced PD173074-mediated fibroblast growth factor receptor (FGFR) inhibition and cytotoxicity. In conclusion, intrinsic fluorescence enables analysis of molecular factors influencing intracellular pharmacokinetics of PD173074. Lysosome-alkalinizing agents might represent candidates for rational combination treatment, preventing cancer cell-intrinsic PD173074 resistance based on lysosomal trapping.
    Sprache Englisch
    Erscheinungsdatum 2018-12-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells7120259
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Fibroblast growth factor receptor 4 promotes glioblastoma progression: a central role of integrin-mediated cell invasiveness.

    Gabler, Lisa / Jaunecker, Carola Nadine / Katz, Sonja / van Schoonhoven, Sushilla / Englinger, Bernhard / Pirker, Christine / Mohr, Thomas / Vician, Petra / Stojanovic, Mirjana / Woitzuck, Valentin / Laemmerer, Anna / Kirchhofer, Dominik / Mayr, Lisa / LaFranca, Mery / Erhart, Friedrich / Grissenberger, Sarah / Wenninger-Weinzierl, Andrea / Sturtzel, Caterina / Kiesel, Barbara /
    Lang, Alexandra / Marian, Brigitte / Grasl-Kraupp, Bettina / Distel, Martin / Schüler, Julia / Gojo, Johannes / Grusch, Michael / Spiegl-Kreinecker, Sabine / Donoghue, Daniel J / Lötsch, Daniela / Berger, Walter

    Acta neuropathologica communications

    2022  Band 10, Heft 1, Seite(n) 65

    Abstract: Glioblastoma (GBM) is characterized by a particularly invasive phenotype, supported by oncogenic signals from the fibroblast growth factor (FGF)/ FGF receptor (FGFR) network. However, a possible role of FGFR4 remained elusive so far. Several ... ...

    Abstract Glioblastoma (GBM) is characterized by a particularly invasive phenotype, supported by oncogenic signals from the fibroblast growth factor (FGF)/ FGF receptor (FGFR) network. However, a possible role of FGFR4 remained elusive so far. Several transcriptomic glioma datasets were analyzed. An extended panel of primary surgical specimen-derived and immortalized GBM (stem)cell models and original tumor tissues were screened for FGFR4 expression. GBM models engineered for wild-type and dominant-negative FGFR4 overexpression were investigated regarding aggressiveness and xenograft formation. Gene set enrichment analyses of FGFR4-modulated GBM models were compared to patient-derived datasets. Despite widely absent in adult brain, FGFR4 mRNA was distinctly expressed in embryonic neural stem cells and significantly upregulated in glioblastoma. Pronounced FGFR4 overexpression defined a distinct GBM patient subgroup with dismal prognosis. Expression levels of FGFR4 and its specific ligands FGF19/FGF23 correlated both in vitro and in vivo and were progressively upregulated in the vast majority of recurrent tumors. Based on overexpression/blockade experiments in respective GBM models, a central pro-oncogenic function of FGFR4 concerning viability, adhesion, migration, and clonogenicity was identified. Expression of dominant-negative FGFR4 resulted in diminished (subcutaneous) or blocked (orthotopic) GBM xenograft formation in the mouse and reduced invasiveness in zebrafish xenotransplantation models. In vitro and in vivo data consistently revealed distinct FGFR4 and integrin/extracellular matrix interactions. Accordingly, FGFR4 blockade profoundly sensitized FGFR4-overexpressing GBM models towards integrin/focal adhesion kinase inhibitors. Collectively, FGFR4 overexpression contributes to the malignant phenotype of a highly aggressive GBM subgroup and is associated with integrin-related therapeutic vulnerabilities.
    Mesh-Begriff(e) Animals ; Carcinogenesis ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Integrins ; Mice ; Neoplasm Recurrence, Local ; Receptor, Fibroblast Growth Factor, Type 4/genetics ; Receptor, Fibroblast Growth Factor, Type 4/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins
    Chemische Substanzen Integrins ; Zebrafish Proteins ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1) ; fgfr4 protein, zebrafish (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2022-04-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-022-01363-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Targeting fibroblast growth factor receptors to combat aggressive ependymoma.

    Lötsch, Daniela / Kirchhofer, Dominik / Englinger, Bernhard / Jiang, Li / Okonechnikov, Konstantin / Senfter, Daniel / Laemmerer, Anna / Gabler, Lisa / Pirker, Christine / Donson, Andrew M / Bannauer, Peter / Korbel, Pia / Jaunecker, Carola N / Hübner, Jens-Martin / Mayr, Lisa / Madlener, Sibylle / Schmook, Maria T / Ricken, Gerda / Maaß, Kendra /
    Grusch, Michael / Holzmann, Klaus / Grasl-Kraupp, Bettina / Spiegl-Kreinecker, Sabine / Hsu, Jennifer / Dorfer, Christian / Rössler, Karl / Azizi, Amedeo A / Foreman, Nicholas K / Peyrl, Andreas / Haberler, Christine / Czech, Thomas / Slavc, Irene / Filbin, Mariella G / Pajtler, Kristian W / Kool, Marcel / Berger, Walter / Gojo, Johannes

    Acta neuropathologica

    2021  Band 142, Heft 2, Seite(n) 339–360

    Abstract: Ependymomas (EPN) are central nervous system tumors comprising both aggressive and more benign molecular subtypes. However, therapy of the high-risk subtypes posterior fossa group A (PF-A) and supratentorial RELA-fusion positive (ST-RELA) is limited to ... ...

    Abstract Ependymomas (EPN) are central nervous system tumors comprising both aggressive and more benign molecular subtypes. However, therapy of the high-risk subtypes posterior fossa group A (PF-A) and supratentorial RELA-fusion positive (ST-RELA) is limited to gross total resection and radiotherapy, as effective systemic treatment concepts are still lacking. We have recently described fibroblast growth factor receptors 1 and 3 (FGFR1/FGFR3) as oncogenic drivers of EPN. However, the underlying molecular mechanisms and their potential as therapeutic targets have not yet been investigated in detail. Making use of transcriptomic data across 467 EPN tissues, we found that FGFR1 and FGFR3 were both widely expressed across all molecular groups. FGFR3 mRNA levels were enriched in ST-RELA showing the highest expression among EPN as well as other brain tumors. We further identified high expression levels of fibroblast growth factor 1 and 2 (FGF1, FGF2) across all EPN subtypes while FGF9 was elevated in ST-EPN. Interrogation of our EPN single-cell RNA-sequencing data revealed that FGFR3 was further enriched in cycling and progenitor-like cell populations. Corroboratively, we found FGFR3 to be predominantly expressed in radial glia cells in both mouse embryonal and human brain datasets. Moreover, we detected alternative splicing of the FGFR1/3-IIIc variant, which is known to enhance ligand affinity and FGFR signaling. Dominant-negative interruption of FGFR1/3 activation in PF-A and ST-RELA cell models demonstrated inhibition of key oncogenic pathways leading to reduced cell growth and stem cell characteristics. To explore the feasibility of therapeutically targeting FGFR, we tested a panel of FGFR inhibitors in 12 patient-derived EPN cell models revealing sensitivity in the low-micromolar to nano-molar range. Finally, we gain the first clinical evidence for the activity of the FGFR inhibitor nintedanib in the treatment of a patient with recurrent ST-RELA. Together, these preclinical and clinical data suggest FGFR inhibition as a novel and feasible approach to combat aggressive EPN.
    Mesh-Begriff(e) Animals ; Central Nervous System Neoplasms/genetics ; Central Nervous System Neoplasms/pathology ; Ependymoma/genetics ; Ependymoma/pathology ; Humans ; Mice ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; Receptor, Fibroblast Growth Factor, Type 3/metabolism ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism
    Chemische Substanzen Receptors, Fibroblast Growth Factor ; FGFR1 protein, human (EC 2.7.10.1) ; FGFR3 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2021-05-27
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-021-02327-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Cerebrospinal Fluid Penetration and Combination Therapy of Entrectinib for Disseminated

    Mayr, Lisa / Guntner, Armin S / Madlener, Sibylle / Schmook, Maria T / Peyrl, Andreas / Azizi, Amedeo A / Dieckmann, Karin / Reisinger, Dominik / Stepien, Natalia M / Schramm, Kathrin / Laemmerer, Anna / Jones, David T W / Ecker, Jonas / Sahm, Felix / Milde, Till / Pajtler, Kristian W / Blattner-Johnson, Mirjam / Strbac, Miroslav / Dorfer, Christian /
    Czech, Thomas / Kirchhofer, Dominik / Gabler, Lisa / Berger, Walter / Haberler, Christine / Müllauer, Leonhard / Buchberger, Wolfgang / Slavc, Irene / Lötsch-Gojo, Daniela / Gojo, Johannes

    Journal of personalized medicine

    2020  Band 10, Heft 4

    Abstract: Targeting oncogenic fusion-genes in pediatric high-grade gliomas (pHGG) with entrectinib has emerged as a highly promising therapeutic approach. Despite ongoing clinical studies, to date, no reports on the treatment of cerebrospinal fluid (CSF) ... ...

    Abstract Targeting oncogenic fusion-genes in pediatric high-grade gliomas (pHGG) with entrectinib has emerged as a highly promising therapeutic approach. Despite ongoing clinical studies, to date, no reports on the treatment of cerebrospinal fluid (CSF) disseminated fusion-positive pHGG exist. Moreover, clinically important information of combination with other treatment modalities such as intrathecal therapy, radiotherapy and other targeted agents is missing. We report on our clinical experience of entrectinib therapy in two CSF disseminated
    Sprache Englisch
    Erscheinungsdatum 2020-12-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2662248-8
    ISSN 2075-4426
    ISSN 2075-4426
    DOI 10.3390/jpm10040290
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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