Chromosome‐9 loss detected by fluorescence in situ hybridization in bladder cancer

Abstract

A loss of chromosome‐9 material is one of the most frequent genomic aberrations known in bladder cancer. In order to better understand the role of chromosome‐9 losses in bladder cancer, 125 formalin‐fixed and 37 unfixed bladder tumors were examined using fluorescence in situ hybridization (FISH). A repetitive probe for a pericentromeric region on 9q12 (pHUR98) was applied for chromosome‐9 copy‐number enumeration. Under‐representation of chromosome 9 was found in 74 of 162 cases. There was no association between loss of chromosome 9 and increased grade or stage, papillary growth pattern, p53 protein expression, or tumor‐cell proliferation (Ki‐67). These data show that chromosome‐9 loss is an early event in bladder‐cancer development, occuring independently of p53 alterations. In order to determine the prevalence of large sub‐regional chromosome‐9 deletions, dual hybridizations with pHUR 98 and cosmid probes for 9q34, 9q22, and 9p21 were performed. Partial deletion was detected in only 1 of 36 cases for 9q34 and in 1 of 24 cases for 9p21. Surprisingly, amplification of the interferon alpha locus on 9p21 was seen in 1 of 24 tumors. The finding of 9p amplification may indicate the site of an oncogene relevant for bladder cancer.