Brick by brick: metabolism and tumor cell growth.

By Ralph J. Deberardinis, Nabil Sayed, D. Ditsworth, Craig B. Thompson. Current Opinion in Genetics and Development, 2008

1,028 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/51f533108417912a86c6cf4917192e0865e89e75

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Citations in the corpus

Q's next: The diverse functions of glutamine in metabolism, cell biology and cancer (2009, background): “The potential advantages of this form of metabolism for proliferating cells have been reviewed (DeBerardinis et al., 2008a).”
The impact of O2 availability on human cancer (2008, background): “This hypothesis appears to be incorrect, but a number of other molecular mechanisms promoting 'aerobic glycolysis' have been proposed, including mutations and epigenetic changes in genes encoding tumour suppressors (for example, TP53 ), activation of oncogenes (such as MYC ) and hypoxic adapta”
The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, background): “Hence, diverting the energy flux towards the non-oxidative branch of the PPP has the key advantage of enabling the needed nucleotide biosynthesis through the production of ribose 5-phosphate (Deberardinis et al., 2008).”
Regulation of Immune Responses by mTOR (2011, background): “Instead, lymphocytes utilize oxidative glycolysis, the so-called Warburg effect, to generate ATP (55).”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “…which characteristics of metabolic enzymes, upstream regulating molecules and downstream metabolic products, known as metabolites, are altered (DeBerardinis et al., 2008b; Heiden et al., 2009; Jones and Thompson, 2009; Hanahan and Weinberg, 2011; DeBerardinis and Thompson, 2012; Hirschey et…”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “This result suggests that the deregulation of lipid metabolism extends beyond the commonly noted elevation of lipogenic enzyme levels (ACL, ACC, FAS) (82), and offers the possibility that distinct mechanisms of fatty acid production feed into different downstream pathways.”
Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B-cells (2012, positive): “Although increased glucose metabolism has been hypothesized to drive the bioenergetic needs of cancer cells, it is clear that highly proliferative cancer cells require additional supplies of biosynthetic precursors not met by glucose metabolism; thus there is the requirement of anaplerosis via gluta”
Monoacylglycerol lipase regulates a fatty acid network that promotes cancer pathogenesis (2010, background): “Many other features of lipid biochemistry, however, are also critical for supporting the malignancy of cancer cells, including: 1) the generation of building blocks for newly synthesized membranes to accommodate high rates of proliferation (DeBerardinis et al., 2008; Deberardinis et al., 2008), 2) t”
Pyruvate Kinase M2 Regulates Gene Transcription by Acting as A Protein Kinase (2012, positive): “source from glucose for biosynthesis (Christofk et al., 2008a; Deberardinis et al., 2008; Garber, 2006; Mazurek and Eigenbrodt, 2003).”
Targeting cellular metabolism to improve cancer therapeutics (2013, background): “There are two types of GLS in mammalian cells, kidney-type GLS (GLS1) and liver-type GLS (GLS2).(98) Metabolic flux experiments tracking (13)C show that cancer cells exhibiting Warburg-like metabolism do not stop utilizing the TCA cycle”
Hypoxic and Ras-transformed cells support growth by scavenging unsaturated fatty acids from lysophospholipids (2013, background): “Oncogenes actively reprogram metabolism to facilitate this supply (1, 2).”
Analysis of cancer metabolism by imaging hyperpolarized nuclei: prospects for translation to clinical research. (2011, background): “The allocation of carbon from glucose and other nutrients into these pathways is determined by a combination of extrinsic and intrinsic modifiers of metabolism and ultimately determines whether tumor cells die or survive and whether they remain quiescent or undergo growth and proliferation [1].”
Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species (2010, background): “, catabolism of glutamine to generate ATP and lactate in the mitochondria) are known to increase in tumors (1, 16).”