Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Posted: Thu Oct 22, 2015 3:02 pm
Cancer Cell. Author manuscript; available in PMC 2013 Mar 20.
Published in final edited form as:
Cancer Cell. 2012 Mar 20; 21(3): 297–308.
doi: 10.1016/j.ccr.2012.02.014
PMCID: PMC3311998
NIHMSID: NIHMS360138
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Patrick S. Ward1,2 and Craig B. Thompson1,*
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Abstract
Cancer metabolism has long been equated with aerobic glycolysis, seen by early biochemists as primitive and inefficient. Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria, but result from oncogene-directed metabolic reprogramming required to support anabolic growth. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation. No longer can cancer-associated alterations in metabolism be viewed as an indirect response to cell proliferation and survival signals. We contend that altered metabolism has attained the status of a core hallmark of cancer.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311998/
Published in final edited form as:
Cancer Cell. 2012 Mar 20; 21(3): 297–308.
doi: 10.1016/j.ccr.2012.02.014
PMCID: PMC3311998
NIHMSID: NIHMS360138
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Patrick S. Ward1,2 and Craig B. Thompson1,*
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at Cancer Cell
See other articles in PMC that cite the published article.
Go to:
Abstract
Cancer metabolism has long been equated with aerobic glycolysis, seen by early biochemists as primitive and inefficient. Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria, but result from oncogene-directed metabolic reprogramming required to support anabolic growth. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation. No longer can cancer-associated alterations in metabolism be viewed as an indirect response to cell proliferation and survival signals. We contend that altered metabolism has attained the status of a core hallmark of cancer.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311998/