Bladder cancer manifests many different forms, ranging from superficia
l to aggressive muscle invasion, which suggests that various genetic a
lterations are responsible. Several attempts have been made to establi
sh correlations between specific genetic alterations and various grade
s of the disease. Numerous types of chromosomal abnormalities have bee
n observed, involving [1p, 1q, 2q, 3p, 4p, 5q, i(5p), +7, +8, 8p, 9p,
9q, 10q23-25, 11p, 11q, +11, 13q, 14q, 17p, 18q, 21q, and Y]. In addit
ion, p53 mutations and loss of heterozygosity on various chromosomes h
ave recently begun to shed light on the molecular pathways of transiti
onal cell carcinomas of the bladder. We have begun to focus on specifi
c genomic sites (especially 9q), although the heterogeneity of the dis
ease and the variable presentation suggests divergent progression path
ways. When the genetic basis of bladder cancer is fully understood, ne
w diagnostic and therapeutic strategies will be developed, which in tu
rn may promote better clinical management by pathologists and urologis
ts.