Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8429307 | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer | 2018 | 12 Pages |
Abstract
Tumors cells reprogram their metabolism to fuel rapid growth. The ability to trace nutrient fluxes in the context of specific alterations has provided new mechanistic insight into the process of oncogenic transformation. A broad array of complementary genetic, epigenetic, transcriptional and translational mechanisms has been identified, revealing a metabolic landscape of cancer. However, cancer metabolism is not a static or uniform process, including within a single tumor. Tumor cells adapt to changing environmental conditions, profoundly shaping the enzymatic dependencies of individual cells. The underlying molecular mechanisms of adaptation, and the specific interactions between tumor genotype, oncogenic signaling, and tissue/biochemical context, remain incompletely understood. In this review, we examine dynamic aspects of how metabolic dependencies develop in cancer, shaped both by genotype and biochemical environment, and review how these interlaced processes generate targetable metabolic vulnerabilities. This article is part of a Special Issue entitled: Cancer Metabolism edited by Dr. Chi Van Dang.
Keywords
mTORC1/2GBMMTABCAAsPHDSCNAMTAPMethylthioadenosine phosphorylaseTCALXRSDHxCTα-KGIDH1/2PRMT5AMLSomatic copy number alterationExtrachromosomal DNAROSα-ketoglutaratePancreatic ductal adenocarcinomaPDAC یا pancreatic ductal adenocarcinomabranched-chain amino acidstricarboxylic acidBBBNSCLCCancer metabolismsuccinate dehydrogenaseOncogenic signalingfumarate hydrataseacute myeloid leukemiaBlood-brain barrierHeterogeneityProtein arginine methyltransferase 5Prolyl hydroxylasenon-small cell lung carcinomaliver X receptorGlioblastoma multiformeReactive oxygen species
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Authors
Junfeng Bi, Sihan Wu, Wenjing Zhang, Paul S. Mischel,