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TGF-beta2 suppression by the antisense oligonucleotide AP 12009 as therapy for high-grade glioma: safety and efficacy results of phase I/II clinical studies

P Hau, U Bogdahn, A Brawanski, D Freudenstein, M Goldbrunner, W Grisold, T Hundsberger, D Koch, H Kostron, M Kunst, M Mehdorn, J Meixensberger, J Pichler, G Schackert, J Schlaier, R Schlingensiepen, S Schmaus, T Schneider, L Spitznagel, G Stauder, G Stockhamm… · Aktuelle Neurologie · 2004 · Heft 09

Dokument
851643
CareLit-ID
Jahr
2004
Publikation
PDF
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Metadaten
DOI
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Bibliografische Angaben

Zeitschrift
Aktuelle Neurologie
Autor:innen
P Hau, U Bogdahn, A Brawanski, D Freudenstein, M Goldbrunner, W Grisold, T Hundsberger, D Koch, H Kostron, M Kunst, M Mehdorn, J Meixensberger, J Pichler, G Schackert, J Schlaier, R Schlingensiepen, S Schmaus, T Schneider, L Spitznagel, G Stauder, G Stockhamm…
Ausgabe
Heft 09 / 2004
Seiten
–
Erschienen: 2004-09-07 00:00:00
ISSN
0302-4350

Zusammenfassung

Background: Tumor derived transforming growth factor beta (TGF-beta) is a pivotal factor for malignant progression by inducing metastasis, angiogenesis, tumor cell proliferation and immunosuppression. High-grade gliomas are highly aggressive tumors showing marked overexpression of the TGF-beta2 isoform which is correlated with advanced tumor stage. Methods: In 3 phase I/II dose escalation studies adult high-grade glioma patients (WHO grades III/IV) with recurrent tumor and evidence of tumor progression on MRI were treated with AP 12009, a TGF-beta2 specific phosphorothioate antisense oligonucleotide. AP 12009 wa…

Schlagworte

Aktuelle Neurologie