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TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis

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TLDR
expression of TIGAR may modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired, and the decrease of intracellular ROS levels in response to TIGar may also play a role in the ability of p53 to protect from the accumulation of genomic damage.
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This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1803 citations till now. The article focuses on the topics: TP53-inducible glycolysis and apoptosis regulator & Apoptosis Regulator.

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Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate

TL;DR: It is argued that altered metabolism has attained the status of a core hallmark of cancer.
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Otto Warburg's contributions to current concepts of cancer metabolism

TL;DR: Otto Warburg's observations are re-examine in relation to the current concepts of cancer metabolism as being intimately linked to alterations of mitochondrial DNA, oncogenes and tumour suppressors, and thus readily exploitable for cancer therapy.
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p53 in health and disease.

TL;DR: It is now becoming clear that p53 can have a much broader role and can contribute to the development, life expectancy and overall fitness of an organism.
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Cancer Cell Metabolism: Warburg and Beyond

TL;DR: The Warburg effect of aerobic glycolysis is re-examine and a framework for understanding its contribution to the altered metabolism of cancer cells is established.
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Tumor Cell Metabolism: Cancer's Achilles' Heel

TL;DR: The peculiarities of tumor cell metabolism are reviewed to discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.
References
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Journal ArticleDOI

On the origin of cancer cells.

Origin of cancer cells

Otto Warburg
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Surfing the p53 network

TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.

TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
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Live or let die: the cell's response to p53

TL;DR: Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.
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