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The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.
TLDR
This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types and regulates regulation of these fluxes by cellular mediators of signal transduction and gene expression.
Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction
TLDR
It is reported that the transcriptional regulatory properties of the oncogene Myc coordinate the expression of genes necessary for cells to engage in glutamine catabolism that exceeds the cellular requirement for protein and nucleotide biosynthesis, resulting in the reprogramming of mitochondrial metabolism to depend on glutaminolysis to sustain cellular viability and TCA cycle anapleurosis.
Beyond aerobic glycolysis: Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis
TLDR
Transformed cells exhibit a high rate of glutamine consumption that cannot be explained by the nitrogen demand imposed by nucleotide synthesis or maintenance of nonessential amino acid pools, and glutamine metabolism provides a carbon source that facilitates the cell's ability to use glucose-derived carbon and TCA cycle intermediates as biosynthetic precursors.
High Frequency Retrotransposition in Cultured Mammalian Cells
TLDR
It is shown that two human L1 elements (L1.2 and LRE2) can actively retrotranspose in cultured mammalian cells, suggesting a potential role for L1-based vectors in random insertional mutagenesis.
The distinct metabolic profile of hematopoietic stem cells reflects their location in a hypoxic niche.
TLDR
It is shown that LT-HSCs utilize glycolysis instead of mitochondrial oxidative phosphorylation to meet their energy demands and that Meis1 regulates HSC metabolism through transcriptional activation of Hif-1alpha.
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
TLDR
An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
Q's next: the diverse functions of glutamine in metabolism, cell biology and cancer
TLDR
The protean roles of glutamine in cancer are reviewed, both in the direct support of tumor growth and in mediating some of the complex effects on whole-body metabolism that are characteristic of tumor progression.
Brick by brick: metabolism and tumor cell growth.
TLDR
This review discusses how tumor cells achieve high rates of nucleotide and fatty acid synthesis, how oncogenes and tumor suppressors influence these activities, and how glutamine metabolism enables macromolecular synthesis in proliferating cells.
Fundamentals of cancer metabolism
TLDR
A conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis will progressively support the development of new strategies to treat human cancer.
Toll-like receptor-induced changes in glycolytic metabolism regulate dendritic cell activation.
TLDR
It is demonstrated that, in mouse DCs, TLR agonists stimulate a profound metabolic transition to aerobic glycolysis, similar to the Warburg metabolism displayed by cancer cells.
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