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Cancers 2010, 2(2), 1013-1026;

Molecular Mechanisms Involved in the Antitumor Activity of Cannabinoids on Gliomas: Role for Oxidative Stress

Department of Pharmacology, Chemotherapy and Toxicology, University of Milan, Via Vanvitelli 32, 20129 Milan, Italy
Department of Structural and Functional Biology, Section of Pharmacology, Center of Neuroscience, University of Insubria, Via A. da Giussano 10, 20152 Busto Arsizio, Varese, Italy
Author to whom correspondence should be addressed.
Received: 8 April 2010 / Revised: 14 May 2010 / Accepted: 17 May 2010 / Published: 26 May 2010
(This article belongs to the Special Issue Oxidative Stress and Cancer)
Full-Text   |   PDF [216 KB, uploaded 26 May 2010]


Cannabinoids, the active components of Cannabis sativa, have been shown to exert antiproliferative and proapoptotic effects on a wide spectrum of tumor cells and tissues. Of interest, cannabinoids have displayed great potency in reducing the growth of glioma tumors, one of the most aggressive CNS tumors, either in vitro or in animal experimental models curbing the growth of xenografts generated by subcutaneous or intrathecal injection of glioma cells in immune-deficient mice. Cannabinoids appear to be selective antitumoral agents as they kill glioma cells without affecting the viability of non-transformed cells. This review will summarize the anti-cancer properties that cannabinoids exert on gliomas and discuss their potential action mechanisms that appear complex, involving modulation of multiple key cell signaling pathways and induction of oxidative stress in glioma cells. View Full-Text
Keywords: cannabinoids; gliomas; apoptosis; cellular mechanism; oxidative stress cannabinoids; gliomas; apoptosis; cellular mechanism; oxidative stress
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Massi, P.; Valenti, M.; Solinas, M.; Parolaro, D. Molecular Mechanisms Involved in the Antitumor Activity of Cannabinoids on Gliomas: Role for Oxidative Stress. Cancers 2010, 2, 1013-1026.

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