With the exception of the gain of chromosome material from 19p observed in three cases (2228–99, 476–98, and 479–98), almost all changes detected in our series (complete or partial loss of 1p, 8p, 9p, and 13q, and gain of 5p, 17q, and 20q) have been previously reported as recurrent genetic changes in chemically induced TCC of the bladder [9]. However, the gain of 19p should be interpreted with caution since this chromosome is prone to hybridization variability that may result in CGH artifacts. For the latter aberrations, the available data therefore indicate that they form part of a pathogenetic pathway followed by both BAC and chemical carcinogen-induced BC. A previous study reported homozygous deletions at 9p without any involvement of 9q in 92% of bilharzial carcinomas obtained from Egyptian patients compared with only 10% in bladder TCC obtained from Swedish patients [19]. In the same study, the type and position of TP53 mutations also differed between the two tumor types, again suggesting molecular differences in the genetic mechanisms of bladder carcinogenesis depending on underlying etiology. Tsutsumi et al. [21] also suggested that loss of 9p21 heterozygosity was associated with early carcinogenesis of SCC of the bladder; they observed homozygous deletion of p16/p19 in 45% of squamous metaplasia from bladder cancer patients, demonstrating that this change occurred already in preneoplastic cells. Muscheck et al. [26] reached the same conclusion, and showed that different histologic subgroups of bladder tumors are characterized by distinct patterns of chromosomal alterations. The loss of 9p we observed in bilharzia-associated lesions is therefore in complete agreement with earlier findings [19-25] and could be an indication that bladder carcinogenesis with this etiology follows a more narrow pathogenetic pathway (loss of 9p) than is the case for BC in the industrialized world (the earliest genomic change in these tumors is loss of 9p, loss of 9q or loss of the entire chromosome).