Etoposide-mediated glioblastoma cell death: dependent or independent on the expression of its target, topoisomerase II alpha?

Sevim, HATİCE; Parkinson, J.; McDonald, K.

doi:10.1007/s00432-011-1046-5

Etoposide-mediated glioblastoma cell death: dependent or independent on the expression of its target, topoisomerase II alpha?

Atıf İçin Kopyala

Sevim H., Parkinson J. F., McDonald K. L.

JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, cilt.137, sa.11, ss.1705-1712, 2011 (SCI-Expanded)

Yayın Türü: Makale / Tam Makale
Cilt numarası: 137 Sayı: 11
Basım Tarihi: 2011
Doi Numarası: 10.1007/s00432-011-1046-5
Dergi Adı: JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
Sayfa Sayıları: ss.1705-1712
Recep Tayyip Erdoğan Üniversitesi Adresli: Hayır

Özet

Treatments which significantly improve progression-free and overall survival for patients with relapsed glioblastoma (GBM) after the standard therapy are lacking. The Topoisomerase II (TopoII) enzyme is a key target of anticancer agents because of the important role it plays in transcription regulation and chromatin remodeling. A drug with strong topoisomerase-mediated anticancer activity is etoposide that is used in combination with carboplatin in patients with relapsed GBM. We hypothesized that tumors harboring high expression of TopoII alpha (TopoIIa) would be more sensitive to etoposide treatment.