Chromosome 9 and 17 aberrations and p53 gene deletion detected by fluorescence in situ hybridization in renal-cell carcinoma.

Abstract

BACKGROUND AND PURPOSE Nuclear grade and tumor stage have been reported as important prognostic factors for renal-cell carcinoma (RCC), but tumors of similar stage and grade can still exhibit wide variations in biologic behavior and clinical outcome. Fluorescence in situ hybridization (FISH) has recently been applied to RCC. This study was designed to investigate whether aberrations of some chromosomes or genes detected by FISH are related to the progression of RCC. MATERIALS AND METHODS We examined 52 patients with RCC, including 31 patients without metastasis (control group) and 21 patients with either concurrent or subsequent metastasis (metastatic group). Paraffin-embedded specimens of the primary tumors were analyzed by FISH for aberrations of chromosomes 9 and 17, as well as for p53 gene alterations. RESULTS The incidence of aberrations of chromosome 9 was higher in the metastatic group than in the control group. The p53 gene deletion rate was significantly higher in the metastatic group than in the control group. When the metastatic group was separated into concurrent and subsequent metastasis subgroups, chromosome 17 aberrations as well as p53 gene deletion were significantly more common in the subsequent metastasis group than in the control group. CONCLUSIONS Numerical aberrations of chromosome 17 as well as p53 gene deletion detected by FISH may be markers of chromosomal instability in RCC and are probably associated with an increased propensity to metastasize.