Molecular cytogenetic identification of cyclin D1 gene amplification in a renal pelvic tumor attributed to phenacetin abuse

Despite extensive epidemiologic evidence of phenacetin abuse as a risk fact or for renal pelvic carcinomas, genetic alterations in the resultant tumors remain largely unclear. In this report, a phenacetin-associated renal pelv ic carcinoma (histologically a transitional-cell carcinoma) from an 80-year -old female patient was evaluated by molecular cytogenetic methods. Fluores cence in situ hybridization was used to identify chromosome gains or tosses for the cyclin DI, p53, Rb and c-myc genes and the ploidy of their respect ive chromosomes. Cyclin Df gene amplification, but normal copy numbers of p 53, Rb and c-myc, and normal ploidy of chromosomes 8, 11, 13 and 17 were ob served. Expression of cyclin D1 protein was confirmed by immunohistochemist ry. In the absence of p53, Rb or c-myc abnormalities, the results suggested that cyclin DI gene amplification and its protein overexpression may be in volved in the genesis of renal pelvic carcinomas associated with phenacetin abuse.