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Maintenance of EGFR and EGFRvIII expressions in an in vivo and in vitro model of human glioblastoma multiforme

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  1. A programmed wave of uridylation-primed mRNA degradation is essential for meiotic progression and mammalian spermatogenesis

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  2. Hepatitis B virus upregulates host microRNAs that target apoptosis-regulatory genes in an in vitro cell model

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  3. uPARAP/endo180 directs lysosomal delivery and degradation of collagen IV

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  4. Localization of urokinase-type plasminogen activator receptor on U937 cells: phorbol ester PMA induces heterogeneity

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  1. Identification of Tumor Antigens Among the HLA Peptidomes of Glioblastoma Tumors and Plasma

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  2. Withdrawal: Identification of tumor antigens among the HLA peptidomes of glioblastoma tumors and plasma

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  3. Actively personalized vaccination trial for newly diagnosed glioblastoma

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  4. Early Postoperative 18F-FET PET/MRI for Pediatric Brain and Spinal Cord Tumors

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  5. Extracranial metastases in glioblastoma-Two case stories

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Glioblastoma multiforme (GBM) is the most common, and most aggressive primary brain tumor among adults. A vast majority of the tumors express high levels of the epidermal growth factor receptor (EGFR) as a consequence of gene amplification. Furthermore, gene amplification is often associated with mutation of EGFR, and the constitutive activated deletion variant EGFRvIII is the most common EGFR mutation found in GBM. Activated EGFR signaling, through overexpression and/or mutation, is involved in increased tumorigenic potential. As such, EGFR is an attractive target for GBM therapy. However, clinical studies with EGFR inhibitors have shown inconsistent results, and as such, further knowledge regarding the role of EGFR and EGFRvIII in GBM is needed. For this, an appropriate in vivo/in vitro tumor model is required. Here, we report the establishment of an experimental GBM model in which the expressions of EGFR and EGFRvIII are maintained both in xenograft tumors growing subcutaneously on mice and in cell cultures established in stem cell conditions. With this model it will be possible to further study the role of EGFR and EGFRvIII, and response to targeted therapy, in GBM.
Original languageEnglish
JournalExperimental Cell Research
Volume317
Issue number11
Pages (from-to)1513-26
Number of pages14
ISSN0014-4827
DOIs
Publication statusPublished - 1 Jul 2011

ID: 32428052