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Pharmaceuticals 2013, 6(12), 1475-1506; doi:10.3390/ph6121475

Glioblastoma Multiforme Therapy and Mechanisms of Resistance

1
Department of Biochemistry and Molecular Pharmacology and Department of Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
2
School of Pharmacy, University of Bradford, Bradford BD7 1DP, UK
These authors contributed equally to works.
*
Author to whom correspondence should be addressed.
Received: 11 September 2013 / Revised: 4 November 2013 / Accepted: 12 November 2013 / Published: 25 November 2013
(This article belongs to the Special Issue Chemotherapeutic Agents)
View Full-Text   |   Download PDF [315 KB, 26 November 2013; original version 25 November 2013]   |  

Abstract

Glioblastoma multiforme (GBM) is a grade IV brain tumor characterized by a heterogeneous population of cells that are highly infiltrative, angiogenic and resistant to chemotherapy. The current standard of care, comprised of surgical resection followed by radiation and the chemotherapeutic agent temozolomide, only provides patients with a 12–14 month survival period post-diagnosis. Long-term survival for GBM patients remains uncommon as cells with intrinsic or acquired resistance to treatment repopulate the tumor. In this review we will describe the mechanisms of resistance, and how they may be overcome to improve the survival of GBM patients by implementing novel chemotherapy drugs, new drug combinations and new approaches relating to DNA damage, angiogenesis and autophagy. View Full-Text
Keywords: angiogenesis; autophagy; imidazotetrazine; MGMT; DNA repair; temozolomide; cancer stem cells angiogenesis; autophagy; imidazotetrazine; MGMT; DNA repair; temozolomide; cancer stem cells
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Ramirez, Y.P.; Weatherbee, J.L.; Wheelhouse, R.T.; Ross, A.H. Glioblastoma Multiforme Therapy and Mechanisms of Resistance. Pharmaceuticals 2013, 6, 1475-1506.

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