existence of different histologic types of bladder cancer:

sqamous cell carcinoma, herein described

transitional cell carcinoma

adenocarcinoma, rare

poorly differenciated carcinoma/small cell carcinoma, exceptional

most often secondary to bilharzial infection (schistosoma haematobium), may be associated with other types of long term irritations: chronic infections, calculi, treatment with cyclophosphamid

geographic areas of high incidence: represents 70 to 80% of the cases of badder cancer in the Middle East and in Africa, in particular in Egypt, were it is the most common adult cancer; only 5% in Europe and in the USA, where the transitional cell carcinoma represents 90-95 % of cases

grading and staging: tumours are:

graded by the degree of cellular atypia (G0->G3), and

staged: pTIS carcinoma in situ (but high grade), and pTa papillary carcinoma, both mucosally confined; pT1 lamina propria invasive; pT2 infiltrates the superficial muscle, and pT3a, the deep mucle; pT3b invasion into perivesical fat; pT4 extends into neighbouring structures and organs

considered to have a poorer prognosis than the transitional cell carcinoma

highly complex karyotypes, yet poorly known

allelic losses are frequent; the most frequent regions involved in loss of heterozygocity (LOH) are 3p, 8p, 9p, 9q, 17p; the karyotype is more complex in advanced grades/stages, as in transitional cell carcinoma

Chromosome 7: trisomy 7 seems to be more frequent than in transitional cell carcinoma, and is found more often in advanced stages; unknown significance as +7 may also be found in normal tissues

Chromosome 9: monosomy 9 is an early event and might even occur at dysplastic stages; allelic losses are frequent, mainly in 9p (65%), more often than for transitional cell carcinoma; LOH are found in particular in the locus where CDKN2/P16 sits; homozygous deletion of P16 is frequent (50%) and may also be found in squamous metaplasias from cancerous patients (but not in squamous metaplasias from non cancerous patients); trisomy 9, on the other hand, would be frequent in advance diseases

Chromosome 17: P53 is often implicated, especially in high grades/stages; the profile of mutations of P53 is different from what is found in transitional cell carcinoma

comparative genomic hybridization (CGH) and multi-FISH (M-FISH) are complementary tools to determine respectively unbalanced segments and structural rearrangements in these complex karyotypes

multistep process; largely unknown