Analysis of genomic alterations on urological malignancies by fluorescence in situ hybridization

An author (H.M.) had a chance to go abroad to Karolinska Institute, Sweden from 1992 to 94, and learnded molecular cytogenetic techniques. The following results had been obtained and published in the literature: Bradder cancer: Numericalalterations on chromosome 7, 9, and 17 by dual-color fruorescence in situ hybridization (FISH) demonstrated that chromosome 7 trisomy and 9 monosomy were the most frequently occurred not only in the tumor, but also in the surrounding intact bladder mucosa, and that 9 monosomy detected by using negative cytology specimen could predict early recurrence of superficial bladder cancer. Chromosome 17p 13.1 region, on which p53 gene was located, was studied by using cosmid probe, and deletion of these regions had a striking impact on the functional loss of tumor suppresor function in invasive bladder cancer. Immunohistochemical staining of p53 showed clinical significance in predicting patient prognosis in bladder cancer. Prostate cancer: Studies on chromosomal deletion of 8p22, 23-pter, 10q24-qter, and 16q24 demonstrated that 8p deletion had close association with tumor stage as well as pathological grade. Further investigation on Japanese prostate cancer suggested that putative tumor suppressor genes are located on 8p 21.1-21.2 and 21.3-22. Collaborative studies with Karolinska Institute were published that 16q 24 deletion had signficant relation to metastatic ability in prostage cancer, and sporadic prostate cancer arose from mutual influence of those genomic alterations with environmental factors. Further follow-up study proved deletion on 8p22 to a universal genetic marker for disease progression in Japanese prostage cancer as well as Swedish. Renal cell carcinoma: FISH studies on 5q22.3-23.2 demonstrated that gain and loss of 5q22.3-23.2 were predictive genetic marker for favorable and unfavorable patient outcome, respectively in renal cell carcinoma. Cases with 3p loss, the most frequent alteration in renal cell carcinoma, in association with 8q24 (c-myc) gain was significantly higher in high stage tumor. Genetic mapping on chromosome 9 using satellite marker showed frequent deletion in PTCH gene located on 9q22.

FISH

renal cell carcinoma

bladder cancer

prostate cancer

chromosome