Ccr. Lee et al., Molecular cytogenetic identification of cyclin D1 gene amplification in a renal pelvic tumor attributed to phenacetin abuse, PATHOL INT, 49(7), 1999, pp. 648-652
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.