In contrast to the extensive cytogenetic and molecular genetic analyses that exist of bladder TCC in Western countries [9], little is known about the genetic alterations of post-bilharzial BC [10]. Cytogenetic investigations require in vitro culturing of tumor cells and therefore may be difficult to perform in areas with a high frequency of bilharziasis-associated BC (BAC). Comparative genomic hybridization (CGH), on the other hand, is a powerful molecular cytogenetic technique not dependent on the presence of vital cells. The technique utilizes differentially labeled tumor DNA and normal tissue DNA as competing probes and normal metaphases as templates to detect and localize gains and/or losses of genetic material across the entire tumor genome [11]. Although CGH cannot detect balanced chromosomal changes, its ability to identify genomic imbalances even in archival, paraffin-embedded tumor materials [12] makes it uniquely well suited when fresh samples are not available. Accordingly, we planned the present experiment to characterize the genetic defects underlying the development of BAC and to determine if its distinct morphologic and clinical characteristics evolve following genetic alterations different from those detected in BC in industrialized countries.