Several preneoplastic urothelial lesions may precede the development of BAC such as inflammatory polyp, bilharzial granuloma, and bilharzial ulcer. To our knowledge, no data are available on the karyotypic characteristics of these lesions. Preneoplastic lesions in other organs have been shown to harbor nonrandom acquired genetic aberrations; in fibrocystic disease of the breast, for instance, cytogenetic studies have revealed clonal chromosomal abnormalities resembling the ones detected in carcinomas of the same organ [17]. Hence, another objective of the present study was to find out if benign bilharzial bladder lesions also carry chromosomal aberrations, and if they do, whether they resemble those seen in bladder carcinomas. Such changes, if present, would presumably constitute the earliest steps of a putative multistage cascade of post-bilharzial carcinogenesis [18]. Of the 6 non-neoplastic lesions examined, 5 were noninformative, in-as-much as no gains or losses were detected, and only in case 286–98 were chromosomal imbalances seen, one of them loss of 9p. The data are of course meager, but viewed in concert with what has already been reported [19-21], they come across as meaningful. Thus, loss of material from 9p in both malignant and non-malignant bilharzial lesions appears to be an initiating event in BAC. However, several have shown that loss of 9p (without loss of 9q) is a common genetic event in advanced, muscle invasive TCC, and since most (80%) BACs are advanced as far as grade and stage are concerned, loss of material from 9p may be seen more frequently in these carcinomas [22-25].