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Download Biology of Renal Cell Carcinoma by Ronald M. Bukowski M.D., James H. Finke Ph.D., Eric A. Klein PDF

By Ronald M. Bukowski M.D., James H. Finke Ph.D., Eric A. Klein M.D. (auth.)

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Somatic mutations were seen in both localized and advanced tumors. Because we previously failed to detect p53 mutations in these same localized tumors (22) these results indicate that VHL somatic mutation was an early event in tumorigenesis, occurring before other mutations. We identified only a single mutation in any of the renal tumors analyzed. This was expected since most of these tumors were previously analyzed for deletions and shown to have chromosome 3p loss of heterozygosity (LOH). A polymorphism was found in the first exon of the VHL gene, and we were able to assess VHL LOH directly.

And EGFR may play an important role in the progression ofRCC. Interleukin-6 (IL-6), originally identified as a T-cell-derived lymphokine, is now thought to be an autocrine growth factor for RCCs (13). Previously, we reported thatlL-6 expression was detected in 22 of43 RCCs (51 %) (14). Enhanced expression oflL-6 correlated with the clinical stage ofRCC, especially with regard to the presence of lymph node metastasis, and the serum level of C-reactive protein. Therefore, we proposed that the level ofIL-6 expression may be predictive of the malignant potential ofRCC.

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