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Carcinogenesis Advance Access originally published online on March 25, 2009
Carcinogenesis 2009 30(8):1269-1280; doi:10.1093/carcin/bgp070
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Metabolic transformation in cancer

Daniel A. Tennant, Raúl V. Durán, Houda Boulahbel and Eyal Gottlieb*

Cancer Research UK, Beatson Institute for Cancer Research, Glasgow, G61 1BD, UK

* To whom correspondence should be addressed. Tel: +44 1413303981; Fax: +44 1419426521; Email: e.gottlieb{at}beatson.gla.ac.uk

In 2000, Douglas Hanahan and Robert Weinberg published a review detailing the six hallmarks of cancer. These are six phenotypes that a tumour requires in order to become a fully fledged malignancy: persistent growth signals, evasion of apoptosis, insensitivity to anti-growth signals, unlimited replicative potential, angiogenesis and invasion and metastasis. However, it is becoming increasingly clear that these phenotypes do not portray the whole story and that other hallmarks are necessary: one of which is a shift in cellular metabolism. The tumour environment creates a unique collection of stresses to which cells must adapt in order to survive. This environment is formed by the uncontrolled proliferation of cells, which ignore the cues that would create normal tissue architecture. As a result, the cells forming the tumour are exposed to low oxygen and nutrient levels, as well as high levels of toxic cellular waste products, which is thought to propel cells towards a more transformed phenotype, resistant to cell death and pro-metastatic.

Abbreviations: ATP, adenosine triphosphate; ASCT2, alanine serine cysteine transporter 2; COX, cytochrome c oxidase; ETC, electron transport chain; FH, fumarate hydratase; G6P, glucose 6-phosphate; HIF, hypoxia-inducible factor; mtDNA, mitochondrial DNA; mTOR, mammalian target of rapamycin; mTORC, mammalian target of rapamycin complex; NF-{kappa}B, nuclear factor-kappaB; OXPHOS, oxidative phosphorylation; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; PFK, phosphofructokinase 1; PFK2/FBPase, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase; PGM, phosphoglycerate mutase; PHD, prolyl hydroxylase; PK, pyruvate kinase; PPP, pentose phosphate pathway; ROS, reactive oxygen species; SDH, succinate dehydrogenase; TCA, tricarboxylic acid; TIGAR, TP53-induced glycolysis and apoptosis regulator; TSC1/2, tuberosclerosis complex 1/2

Received January 12, 2009; revised March 3, 2009; accepted March 18, 2009.


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