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Decrease of mitochondrial DNA content and energy metabolism in renal cell carcinoma

MPG-Autoren
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Meierhofer,  David
Mass Spectrometry (Head: David Meierhofer), Scientific Service (Head: Christoph Krukenkamp), Max Planck Institute for Molecular Genetics, Max Planck Society;
Department of Pediatrics, Paracelsus Private Medical University Salzburg, A-5020 Salzburg, Austria ;

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Zitation

Meierhofer, D., Mayr, J. A., Foetschl, U., Berger, A., Fink, K., Schmeller, N., et al. (2004). Decrease of mitochondrial DNA content and energy metabolism in renal cell carcinoma. Carcinogenesis, 25(6), 1005-1010. doi:10.1093/carcin/bgh104.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0028-8F5A-0
Zusammenfassung
To elucidate the relationship between tumorgenesis and the mitochondrial energy metabolism in renal neoplasms, we studied three individual enzyme activities of the oxidative phosphorylation, two components of the Krebs cycle and the mitochondrial DNA content of renal carcinomas including 29 conventional, five papillary, two unclassified carcinomas with sarcomatoid features and one collecting duct carcinoma. A significant reduction of all mitochondrial enzyme activities including complex V, as well as of the mitochondrial DNA content was detected in 34 of 37 renal carcinoma tissues as compared with control kidney. Mitochondrial enzyme activities and mitochondrial DNA levels were not statistically different between the conventional, papillary and unclassified sarcomatoid type of renal carcinoma and did not correlate with tumour grade, metastasis, ploidy and proliferative activity as determined by Ki-67 staining. Taken together, our data indicate that a co-ordinated down-regulation of all components necessary for mitochondrial energy metabolism occurs in most renal carcinomas as an early event in carcinoma formation, which does not change with progression of the disease.