Journal ArticleDOI
Glycogen synthase kinase-3β (GSK-3β) and its dysregulation in glioblastoma multiforme
Ryan J. Atkins,Stan S. Stylli,Stan S. Stylli,Rod Luwor,Andrew H. Kaye,Andrew H. Kaye,Christopher M. Hovens +6 more
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TLDR
The activity and function of GSK-3β in a number of signaling pathways and its role in gliomagenesis are reviewed and the need for molecular targeted therapies for GBM patients is identified.About:
This article is published in Journal of Clinical Neuroscience.The article was published on 2013-09-01. It has received 30 citations till now. The article focuses on the topics: GSK-3 & GSK3B.read more
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Inhibition of glycogen synthase kinase-3 beta induces apoptosis and mitotic catastrophe by disrupting centrosome regulation in cancer cells
Yuki Yoshino,Chikashi Ishioka +1 more
TL;DR: It is proposed that centrosome dysregulation is an important mechanism for the anticancer effects of GSK-3β inhibitors and that mitotic catastrophe serves as a safe-guard system to remove cells with any mitotic abnormalities induced by GSK -3β inhibition.
Journal ArticleDOI
Glycogen synthase kinase-3 beta inhibitors as novel cancer treatments and modulators of antitumor immune responses.
Ilyas Sahin,Aditya Eturi,Andre De Souza,Sahithi Pamarthy,Fabio Tavora,Francis J. Giles,Benedito A. Carneiro +6 more
TL;DR: The regulatory role of GSK-3β in apoptosis, cell cycle, DNA repair, tumor growth, invasion, and metastasis reflects the therapeutic relevance of this target and provides the rationale for drug combinations.
Journal ArticleDOI
MicroRNA-101 reverses temozolomide resistance by inhibition of GSK3β in glioblastoma.
TL;DR: It is demonstrated that microRNA-101 (miR-101) can reverse TMZ resistance by inhibition of GSK3β in GBM, thus offer a novel and powerful strategy for GBM therapy.
Journal ArticleDOI
Repair mechanisms help glioblastoma resist treatment
Ryan J. Atkins,Wayne Ng,Wayne Ng,Stanley S. Stylli,Stanley S. Stylli,Christopher M. Hovens,Andrew H. Kaye,Andrew H. Kaye +7 more
TL;DR: Insights into the DNA repair mechanisms that permit resistance to chemoradiotherapy in GBM may help improve patient responses to currently available therapies.
Journal ArticleDOI
Glycogen Synthase Kinase 3β in Cancer Biology and Treatment
TL;DR: The evidence supporting aberrant GSK3β as a hallmark property of cancer is reviewed and the beneficial effects of G SK3β inhibition on normal cells and tissues during cancer therapy are highlighted.
References
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Journal ArticleDOI
Radiotherapy plus Concomitant and Adjuvant Temozolomide for Glioblastoma
Roger Stupp,Warren P. Mason,Martin J. van den Bent,Michael Weller,Barbara Fisher,Martin J.B. Taphoorn,Karl Belanger,Alba A. Brandes,Christine Marosi,Ulrich Bogdahn,Jürgen Curschmann,Robert C. Janzer,Samuel K. Ludwin,Thierry Gorlia,Anouk Allgeier,Denis Lacombe,J. Gregory Cairncross,Elizabeth Eisenhauer,René O. Mirimanoff +18 more
TL;DR: The addition of temozolomide to radiotherapy for newly diagnosed glioblastoma resulted in a clinically meaningful and statistically significant survival benefit with minimal additional toxicity.
Journal ArticleDOI
Glioma stem cells promote radioresistance by preferential activation of the DNA damage response
Shideng Bao,Qiulian Wu,Roger E. McLendon,Yueling Hao,Qing Ming Shi,Anita B. Hjelmeland,Mark W. Dewhirst,Darell D. Bigner,Jeremy N. Rich +8 more
TL;DR: This work shows that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity, and suggests that CD133-positive tumour cells could be the source of tumour recurrence after radiation.
PatentDOI
Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex
TL;DR: In this paper, the rictor-mTOR complex was used to identify compounds which modulate Akt activity mediated by the Rictor mTOR complex and methods for treating or preventing a disorder that is associated with aberrant Akt activation.
Journal ArticleDOI
Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B.
TL;DR: It is shown that agents which prevent the activation of both MAPKAP kinase-1 and p70S6k by insulin in vivo do not block the phosphorylation and inhibition of GSK3, and it is demonstrated that PKB is the product of the proto-oncogene protein kinase B (PKB, also known as Akt/RAC).
Journal ArticleDOI
Identification of c-MYC as a Target of the APC Pathway
Tong-Chuan He,Andrew B. Sparks,Carlo Rago,Heiko Hermeking,Leigh Zawel,Luis T. da Costa,Patrice J. Morin,Bert Vogelstein,Kenneth W. Kinzler +8 more
TL;DR: The c-MYC oncogene is identified as a target gene in this signaling pathway and shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c- MYC promoter.