The clinical ciiurse ot bladder cancer i s not predicted by histological criteria alone. Mutation dt p53, usually accompanied by allelic loss on the other chromosome 17p, lids been implicated as a prohmostic parameter in several tumors, including hladder cancer. We therefore examined 153 bladder cancer samples by fluorescence in situ hybridization (FISH) to assess deletions on chromosome 17p. Probes for a pericentronieric region on 17 and a probe for the p53 Iricus were applied simultaneously. Prevalence of 17p deletion was lnwer i n pTa (4/43), than in pT1 (20/42) or pT2-4 tumors (2X/5X) (p=O.OOOl). There was alsu a strvng ciirrelatirin between 17p deletions and tumor grade. Average centromere 17 copy number was higher in pT1, than in pTa tumora (p=O.MI(Jl) and correlated also with tumor grade, 17p deletions and p53 imniunostaining (CM1). 1711 deletions cnrreldted with p53 imniunoataining when all c a w s were considercd (p=O.OOUS) but not for the suhgriiup of T2-4 tumors. Our findings suggest that p53 niutatirins as well as 17p deletions are early events in bladder cancer, appearing at the time of early invasim (pT1). Funded by CA47537 and Swiss National Science Foundation.
MONITORING RECURRENT BLADDER TUMORS BY FLUORESCENCE I N SI'IU HYBRIDIZATION.