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pubmed-article:19995572pubmed:dateCreated2010-3-10lld:pubmed
pubmed-article:19995572pubmed:abstractTextThe last decade has witnessed a renaissance of Otto Warburg's fundamental hypothesis, which he put forward more than 80 years ago, that mitochondrial malfunction and subsequent stimulation of cellular glucose utilization lead to the development of cancer. Since most tumor cells demonstrate a remarkable resistance to drugs that kill non-malignant cells, the question has arisen whether such resistance might be a consequence of the abnormalities in tumor mitochondria predicted by Warburg. The present review discusses potential mechanisms underlying the upregulation of glycolysis and silencing of mitochondrial activity in cancer cells, and how pharmaceutical intervention in cellular energy metabolism might make tumor cells more susceptible to anti-cancer treatment.lld:pubmed
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pubmed-article:19995572pubmed:authorpubmed-author:GogvadzeVladi...lld:pubmed
pubmed-article:19995572pubmed:authorpubmed-author:OrreniusStenSlld:pubmed
pubmed-article:19995572pubmed:authorpubmed-author:ZhivotovskyBo...lld:pubmed
pubmed-article:19995572pubmed:copyrightInfo2009 Elsevier Ltd. All rights reserved.lld:pubmed
pubmed-article:19995572pubmed:issnTypeElectroniclld:pubmed
pubmed-article:19995572pubmed:volume31lld:pubmed
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pubmed-article:19995572pubmed:pagination60-74lld:pubmed
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pubmed-article:19995572pubmed:year2010lld:pubmed
pubmed-article:19995572pubmed:articleTitleThe Warburg effect and mitochondrial stability in cancer cells.lld:pubmed
pubmed-article:19995572pubmed:affiliationInstitute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, Stockholm SE-17177, Sweden.lld:pubmed
pubmed-article:19995572pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19995572pubmed:publicationTypeReviewlld:pubmed
pubmed-article:19995572pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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