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The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor
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TLDR
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use.Abstract:
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.read more
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Targeting proteomics to investigate metastasis-associated mitochondrial proteins
Hsiu-Chuan Chou,Hong-Lin Chan +1 more
TL;DR: Equipment-based metabolomic analysis now allows the monitoring of disease progression and diagnosis, and newly emerging techniques, including proteomics, redox-proteomics, and metabolomics, are described in this review.
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Cancer Metabolism and Its Therapeutic Implications
TL;DR: Current understanding of cancer metabolism with major focus on glucose and glutamine metabolisms and their potential therapeutic implications are reviewed.
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3-(7-Azaindolyl)-4-indolylmaleimides as a novel class of mutant isocitrate dehydrogenase-1 inhibitors: Design, synthesis, and biological evaluation.
Hu Yuanyuan,Anhui Gao,Honghui Liao,Zhang Mengmeng,Xu Gaoya,Li-Xin Gao,Lei Xu,Yubo Zhou,Jian-Rong Gao,Qing Ye,Jia Li +10 more
TL;DR: Evaluation of the biological activities at the cellular level showed that compounds 11a, 11c, 11e, 11g, and 11s could effectively suppress the production of 2‐hydroxyglutaric acid in U87MG cells expressing IDH1/R132H.
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Advancement in the diagnosis of mitochondrial diseases
TL;DR: This review discusses challenges and problems in mitochondrial disease diagnosis, focusing on the mutational profile of both primary and secondary mitochondrial diseases, and the utilization of next-generation technology and multi-omics strategy to improve the diagnosis.
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Strategies for Comparing Metabolic Profiles: Implications for the Inference of Biochemical Mechanisms from Metabolomics Data
Zhen Qi,Eberhard O. Voit +1 more
TL;DR: The results suggest that relative changes in metabolite levels, which reduce bias toward large metabolite concentrations, are better suited for comparisons of metabolic profiles than absolute changes.
References
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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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Targeting HIF-1 for cancer therapy
TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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An Integrated Genomic Analysis of Human Glioblastoma Multiforme
D. Williams Parsons,Siân Jones,Xiaosong Zhang,Jimmy Lin,Rebecca J. Leary,Philipp Angenendt,Parminder Mankoo,Hannah Carter,I-Mei Siu,Gary L. Gallia,Alessandro Olivi,Roger E. McLendon,B.K. Ahmed Rasheed,Stephen T. Keir,Tatiana Nikolskaya,Yuri Nikolsky,Dana A. Busam,Hanna Tekleab,Luis A. Diaz,James Hartigan,Doug R. Smith,Robert L. Strausberg,Suely Kazue Nagahashi Marie,Sueli Mieko Oba Shinjo,Hai Yan,Gregory J. Riggins,Darell D. Bigner,Rachel Karchin,Nick Papadopoulos,Giovanni Parmigiani,Bert Vogelstein,Victor E. Velculescu,Kenneth W. Kinzler +32 more
TL;DR: Recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival.
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IDH1 and IDH2 Mutations in Gliomas
Hai Yan,D. Williams Parsons,Genglin Jin,Roger E. McLendon,B.K. Ahmed Rasheed,Weishi Yuan,Ivan Kos,Ines Batinic-Haberle,Siân Jones,Gregory J. Riggins,Henry S. Friedman,Allan H. Friedman,David A. Reardon,James E. Herndon,Kenneth W. Kinzler,Victor E. Velculescu,Bert Vogelstein,Darell D. Bigner +17 more
TL;DR: Mutations of NADP(+)-dependent isocitrate dehydrogenases encoded by IDH1 and IDH2 occur in a majority of several types of malignant gliomas.