Linked Life Data

18413815

Source:http://linkedlifedata.com/resource/pubmed/id/18413815

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-4-16
pubmed:abstractText
Many solid tumors exhibit abnormal aerobic metabolism characterized by increased glycolytic capacity and decreased cellular respiration. Recently, mutations in the nuclear encoded mitochondrial enzymes fumarate hydratase and succinate dehydrogenase have been identified in certain tumor types, thus demonstrating a direct link between mitochondrial energy metabolism and tumorigenesis. Although mutations in the mitochondrial genome (mitochondrial DNA, mtDNA) also can affect aerobic metabolism and mtDNA alterations are frequently observed in tumor cells, evidence linking respiratory chain deficiency in a specific tumor type to a specific mtDNA mutation has been lacking.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2270-5
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Loss of complex I due to mitochondrial DNA mutations in renal oncocytoma.
pubmed:affiliation
Department of Pediatrics, University Hospital Salzburg, Paracelsus Medical University, Salzburg, Austria.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't