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Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

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

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DOI

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Mitotic and Proliferative Indices in WHO Grade III Meningioma

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Pharmacokinetic analysis of [68Ga]Ga-DOTA-TOC PET in meningiomas for assessment of in vivo somatostatin receptor subtype 2

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. In vivo imaging of cell proliferation in meningioma using 3'-deoxy-3'-[18F]fluorothymidine PET/MRI

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Novel Clinical and Radiological Findings in a Family with Autosomal Recessive Omodysplasia

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  5. Pearls and Pitfalls in Interpretation of 68Ga-DOTATOC PET Imaging

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Vis graf over relationer
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.
OriginalsprogEngelsk
TidsskriftExperimental Cell Research
Vol/bind317
Udgave nummer11
Sider (fra-til)1513-26
Antal sider14
ISSN0014-4827
DOI
StatusUdgivet - 1 jul. 2011

ID: 32428052