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Cancers 2013, 5(4), 1469-1484; doi:10.3390/cancers5041469

Tumor Metabolism of Malignant Gliomas

 and *
Received: 22 October 2013 / Accepted: 24 October 2013 / Published: 8 November 2013
(This article belongs to the Special Issue Glioblastoma)
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Abstract: Constitutively activated oncogenic signaling via genetic mutations such as in the EGFR/PI3K/Akt and Ras/RAF/MEK pathways has been recognized as a major driver for tumorigenesis in most cancers. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA and RNA, leading to enhanced growth of human tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. In malignant gliomas, metabolism pathways of glucose, glutamine and lipid are significantly reprogrammed. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. In this review, we will summarize recent studies revealing critical gene alterations that lead to metabolic changes in malignant gliomas, and also discuss promising therapeutic strategies via targeting the key players in metabolic regulation.
Keywords: glioblastoma; tumor metabolism; SREBP-1; LDLR; LXR; glucose; lipids; cholesterol glioblastoma; tumor metabolism; SREBP-1; LDLR; LXR; glucose; lipids; cholesterol
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Ru, P.; Williams, T.M.; Chakravarti, A.; Guo, D. Tumor Metabolism of Malignant Gliomas. Cancers 2013, 5, 1469-1484.

AMA Style

Ru P, Williams TM, Chakravarti A, Guo D. Tumor Metabolism of Malignant Gliomas. Cancers. 2013; 5(4):1469-1484.

Chicago/Turabian Style

Ru, Peng; Williams, Terence M.; Chakravarti, Arnab; Guo, Deliang. 2013. "Tumor Metabolism of Malignant Gliomas." Cancers 5, no. 4: 1469-1484.

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