Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-218
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dc.contributor.authorVewinger, Nadine-
dc.contributor.authorHuprich, Sabrina-
dc.contributor.authorSeidmann, Larissa-
dc.contributor.authorRusso, Alexandra-
dc.contributor.authorAlt, Francesca-
dc.contributor.authorBender, Hannah-
dc.contributor.authorSommer, Clemens-
dc.contributor.authorSamuel, David-
dc.contributor.authorLehmann, Nadine-
dc.contributor.authorBackes, Nora-
dc.contributor.authorRoth, Lea-
dc.contributor.authorHarter, Patrick N.-
dc.contributor.authorFilipski, Katharina-
dc.contributor.authorFaber, Jörg-
dc.contributor.authorParet, Claudia-
dc.date.accessioned2019-11-07T14:21:45Z-
dc.date.available2019-11-07T15:21:45Z-
dc.date.issued2019-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/220-
dc.description.abstract(1) Background: The high-grade neuroepithelial tumor of the central nervous system with BCOR alteration (HGNET-BCOR) is a highly malignant tumor. Preclinical models and molecular targets are urgently required for this cancer. Previous data suggest a potential role of insulin-like growth factor (IGF) signaling in HGNET-BCOR. (2) Methods: The primary HGNET-BCOR cells PhKh1 were characterized by western blot, copy number variation, and methylation analysis and by electron microscopy. The expression of IGF2 and IGF1R was assessed by qRT-PCR. The effect of chemotherapeutics and IGF1R inhibitors on PhKh1 proliferation was tested. The phosphorylation of IGF1R and downstream molecules was assessed by western blot. (3) Results: Phkh1 cells showed a DNA methylation profile compatible with the DNA methylation class “HGNET-BCOR” and morphologic features of cellular cannibalism. IGF2 and IGF1R were highly expressed by three HGNET-BCOR tumor samples and PhKh1 cells. PhKh1 cells were particularly sensitive to vincristine, vinblastine, actinomycin D (IC50 < 10 nM for all drugs), and ceritinib (IC50 = 310 nM). Ceritinib was able to abrogate the proliferation of PhKh1 cells and blocked the phosphorylation of IGF1R and AKT. (4) Conclusion: IGF1R is as an attractive target for the development of new therapy protocols for HGNET-BCOR patients, which may include ceritinib and vinblastine.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleIGF1R is a potential new therapeutic target for HGNET-BCOR brain tumor patientsen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-publ-594015-
dc.identifier.doihttp://doi.org/10.25358/openscience-218-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleInternational journal of molecular sciences-
jgu.journal.volume20-
jgu.journal.issue12-
jgu.pages.alternativeArt. 3027-
jgu.publisher.year2019-
jgu.publisher.nameMolecular Diversity Preservation International-
jgu.publisher.placeBasel-
jgu.publisher.urihttp://dx.doi.org/10.3390/ijms20123027-
jgu.publisher.issn1422-0067-
jgu.publisher.issn1661-6596-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2019-11-07T14:21:45Z-
opus.date.modified2019-11-14T09:37:35Z-
opus.date.available2019-11-07T15:21:45-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Universitäres Centrum für Tumorerkrankungen (UCT) Mainzde_DE
opus.organisation.stringFB 04: Medizin: Institut für Neuropathologiede_DE
opus.organisation.stringFB 04: Medizin: Zentrum für Kinder- und Jugendmedizin - Schwerpunkt pädiatrische Kardiologiede_DE
opus.organisation.stringFB 04: Medizin: Institut für Pathologiede_DE
opus.identifier.opusid59401-
opus.institute.number0483-
opus.institute.number0481-
opus.institute.number0470-
opus.institute.number0423-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedSeidmann, Larissa-
opus.affiliatedRusso, Alexandra-
opus.affiliatedAlt, Francesca-
opus.affiliatedSommer, Clemens-
opus.affiliatedBackes, Nora-
opus.affiliatedRoth, Lea-
opus.affiliatedFaber, Jörg-
opus.affiliatedParet, Claudia-
jgu.publisher.doi10.3390/ijms20123027
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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