| pubmed-article:10098401 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10098401 | lifeskim:mentions | umls-concept:C0025519 | lld:lifeskim |
| pubmed-article:10098401 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:10098401 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10098401 | pubmed:dateCreated | 1999-4-27 | lld:pubmed |
| pubmed-article:10098401 | pubmed:abstractText | Over seven decades ago, classical biochemical studies showed that tumors have altered metabolic profiles and display high rates of glucose uptake and glycolysis. Although these metabolic changes are not the fundamental defects that cause cancer, they might confer a common advantage on many different types of cancers, which allows the cells to survive and invade. Recent molecular studies have revealed that several of the multiple genetic alterations that cause tumor development directly affect glycolysis, the cellular response to hypoxia and the ability of tumor cells to recruit new blood vessels. | lld:pubmed |
| pubmed-article:10098401 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10098401 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10098401 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10098401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10098401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10098401 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10098401 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10098401 | pubmed:issn | 0968-0004 | lld:pubmed |
| pubmed-article:10098401 | pubmed:author | pubmed-author:DangC VCV | lld:pubmed |
| pubmed-article:10098401 | pubmed:author | pubmed-author:SemenzaG LGL | lld:pubmed |
| pubmed-article:10098401 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10098401 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:10098401 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10098401 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10098401 | pubmed:pagination | 68-72 | lld:pubmed |
| pubmed-article:10098401 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:10098401 | pubmed:meshHeading | pubmed-meshheading:10098401... | lld:pubmed |
| pubmed-article:10098401 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10098401 | pubmed:articleTitle | Oncogenic alterations of metabolism. | lld:pubmed |
| pubmed-article:10098401 | pubmed:affiliation | Dept of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. cvdang@welchlink.welch.jhu.edu | lld:pubmed |
| pubmed-article:10098401 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10098401 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10098401 | pubmed:publicationType | Review | lld:pubmed |
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