[Loss of heterozygosity fine mapping of chromosome 17p13 in transitional cell carcinoma of human urinary bladder]

Zhonghua Yi Xue Za Zhi. 2002 Feb 10;82(3):161-3.
[Article in Chinese]

Abstract

Objective: To determine the frequency and common deletion region of allelic losses on chromosome 17p13 in transitional cell carcinoma (TCC) of human urinary bladder so as to provide clues for isolation of candidate tumor suppressor genes associated with TCC of urinary bladder.

Methods: Loss of heterozygosity (LOH) analysis was made on 44 samples of surgically resected primary TCC by using 13 microsatellite markers to map the regions frequently deleted on chromosome 17p13. The relationship between the LOH in each locus and pathological grade and stage was analyzed.

Results: Out of the 44 samples, 35 (79.5%) showed allelic loss in at least one of the 17p13 loci. The highest frequency of LOH (41.4%, 12/29) was at D17S513 in 17p13.2, the second highest frequency of LOH (40.5%, 17/42) was at D17S1308 in 17p13.3, and the lowest (14.3%, 4/28) was at D17S261 in 17p13.1. The most frequent LOH loci were mainly located in three regions: D17S695-D17S1308 in 17p13.3, D17S1533-D17S831 in 17p13.2, and TP53 in 17p13.1. Among them only the LOH frequency of TP53 locus was positively correlated to the grade (chi(2) = 5.104, P < 0.05) and stage (chi(2) = 5.382, P < 0.05) of TCC of unrinary bladder.

Conclusion: In 17p13 region, except for TP53 gene, still exist two candidate tumor suppressor genes located in D17S695-D17S1308 and D17S1533-D17S831 involved in the carcinogenesis of TCC of urinary bladder. LOH of TP53 locus may be one of the later events in TCC, and LOH in 17p13.3 and 17p13.2 may be the early events of TCC of uninary bladder.

Publication types

  • English Abstract

MeSH terms

  • Carcinoma, Transitional Cell / genetics*
  • Chromosome Mapping
  • Chromosomes, Human, Pair 17*
  • Disease Progression
  • Gene Deletion
  • Humans
  • Loss of Heterozygosity / genetics*
  • Microsatellite Repeats / genetics
  • Urinary Bladder Neoplasms / genetics*