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

✍ Scribed by Guido Sauter; Holger Moch; Peter Carroll; Russel Kerschmann; Michael J. Mihatsch; Frederic M. Waldman

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: French
• Weight: 674 KB
• Volume: 64
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910640205

✦ Synopsis

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, I25 formalin-fixed and 37 unfixed bladder tumors were examined using fluorescence in situ hybridization (FISH). A repetitive probe for a pericentromeric region on 9q I2 (pHUR98) was applied for chromosome-9 copy-number enumeration. Under-representation of chromosome 9 was found in 74 of I62 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 bladdercancer 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 I of 36 cases for 9q34 and in I of 24 cases for 9 ~2 1 . Surprisingly, amplification of the interferon alpha locus on 9p2 I was seen in I of 24 tumors. The finding of 9p amplification may indicate the site of an oncogene relevant for bladder cancer.