PMID:
     9150947
Authors:
     Sarto C, Marocchi A, Sanchez JC, Giannone D, Frutiger S, Golaz O,
     Wilkins MR, Doro G, Cappellano F, Hughes G, Hochstrasser DF, Mocarelli P.
Title:
     Renal cell carcinoma and normal kidney protein expression.
Journal:
     Electrophoresis. 1997 Mar-Apr;18(3-4):599-604. doi: 10.1002/elps.1150180343.
Abstract:
     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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