Microsatellite instability in transitional cell carcinoma of the urinary tract and its relationship to clinicopathological variables and smoking

✍ Scribed by Toyoaki Uchida; Chunxi Wang; Chieki Wada; Masatsugu Iwamura; Shin Egawa; Ken Koshiba

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: French
• Weight: 420 KB
• Volume: 69
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/(sici)1097-0215(19960422)69:2<142::aid-ijc13>3.0.co;2-b

✦ Synopsis

To determine whether microsatellite instability is involved in the development of transitional cell carcinoma (TCC) of the urinary tract, a microsatellite instability assay was carried out using PCR with 9 microsatellite loci. Thirty-eight TCC samples (30 patients with bladder cancer, 5 with renal pelvic tumors and 3 with ureteral tumors) and I lymph node with metastasis were examined. Microsatellite instability was found in 8 of 38 tumors examined, and 3 showed alterations in more than 2 microsatellite loci. All 8 tumors were beyond grade 2 and stage pT2 advanced tumors. Stages pTI -2 and pT3-4 patients differed significantly. Microsatellite instability was greater in smokers than non-smokers. but the differences were not significant. Microsatellite instability in TCC of the urinary tract is rare in superkial tumors but more common in invasive tumors. Microsatellite alterations would thus appear to occur, and possibly be importantly involved, in the tumorigenesis of urinary tract TCC.

o 1996 WiZey-Liss, Inc.

Bladder cancer is the 5th and 12th most common cancer in the United States and Japan, respectively, the annual incidence rates being approximately 18 and 4.8 cases per 100,000, respectively Japanese Health Welfare Statistics Association, 1991). About 80% of bladder cancer patients exhibit superficial tumors, which often recur and require careful observation and clinical follow-up. Invasive tumors show greater tendency to progress, and patients with such tumors are at high risk of dying, despite radical surgery, radiation and chemotherapy.

Human cancer results from multiple independent genetic changes that activate proto-oncogenes or negate the action of tumor-suppressor genes . Studies on microsatellite instability in hereditary non-polyposis colorectal cancer (HNPCC) strongly indicate the presence of a mutator phenotype (Aaltonen et al.,