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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.

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Metabolic host responses to infection by intracellular bacterial pathogens

TL;DR: There is an urgent need for cellular models that more closely reflect the in vivo infection conditions and the exact knowledge of the metabolic host cell responses may provide new interesting concepts for antibacterial therapies.
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PARP14 promotes the Warburg effect in hepatocellular carcinoma by inhibiting JNK1-dependent PKM2 phosphorylation and activation

TL;DR: It is shown that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP)14 promotes aerobic glycolysis in human hepatocellular carcinoma (HCC) by maintaining low activity of the pyruvate kinase M2 isoform (PKM2), a key regulator of the Warburg effect.
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A Clearer View of the Molecular Complexity of Clear Cell Renal Cell Carcinoma

TL;DR: Recent advances in understanding how dysregulation of the many hypoxia-inducible factor α-dependent and -independent functions of the VHL tumor suppressor protein (pVHL) can contribute to tumor initiation and progression are discussed.
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Therapeutic targeting of cancer cell metabolism

TL;DR: Current concepts of normal metabolism and altered metabolism in cancer cells are reviewed with specific emphasis on molecular targets involved directly in glycolysis or glutamine metabolism, which has been re-discovered as an essential bioenergetic and anabolic substrate for many cancer cell types.
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The embryonic origins of erythropoiesis in mammals.

TL;DR: Some common and distinguishing features of the red blood cell lineages are highlighted and advances in the understanding of how these cells develop and differentiate throughout mammalian ontogeny are summarized.
References
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Journal ArticleDOI

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.

Origin of cancer cells

Otto Warburg
Journal ArticleDOI

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.