Database: PubMed
Entry: 9150947
LinkDB: 9150947
Original site: 9150947 
     Sarto C, Marocchi A, Sanchez JC, Giannone D, Frutiger S, Golaz O,
     Wilkins MR, Doro G, Cappellano F, Hughes G, Hochstrasser DF, Mocarelli P.
     Renal cell carcinoma and normal kidney protein expression.
     Electrophoresis. 1997 Mar-Apr;18(3-4):599-604. doi: 10.1002/elps.1150180343.
     Renal cell carcinoma (RCC), a human kidney cancer from the proximal tubular 
     epithelium, accounts for about 3% of adult malignancies. Molecular and 
     cytogenetic analysis have highlighted deletions, translocations, or loss of 
     heterozygosity in the 3p21-p26, a putative RCC locus, as well as in 6q, 8p, 9pq, 
     and 14pq. Studies on phenotypic expression of human kidney tissue and on 
     post-translational modifications in RCC have not yet provided a marker for early 
     renal cell carcinoma diagnosis. Current diagnostic methods do not help to detect 
     the tumor before advanced stages. We therefore used two-dimensional 
     polyacrylamide gel electrophoresis (2-D PAGE) to study normal and tumor kidney 
     tissues in ten patients suffering from RCC. A human kidney protein map in the 
     SWISS-2DPAGE database accessible through the ExPASy WWW Molecular Biology Server 
     was established. Of 2789 separated polypeptides, 43 were identified by gel 
     comparison, amino acid analysis, N-terminal sequencing, and/or immunodetection. 
     The comparison between normal and tumor kidney tissues showed four polypeptides 
     to be absent in RCC. One of them was identified as ubiquinol cytochrome c 
     reductase (UQCR), whose locus has elsewhere been tentatively assigned to 
     chromosome 19p12 or chromosome 22. A second polypeptide was identified as 
     mitochondrial NADH-ubiquinone oxido-reductase complex I whose locus is located on 
     chromosome 18p11.2 and chromosome 19q13.3. These result suggest that the lack of 
     UQCR and of mitochondrial NADH-ubiquinone oxidoreductase complex I expression in 
     RCC may be caused by unknown deletions, or by changes in gene transcription or 
     translation. It might indicate that mitochondrial disfunction plays a major role 
     in RCC genesis or evolution.

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