## Abstract ## BACKGROUND In the 1999 World Health Organization classification system, papillary tumors of the urinary bladder were classified as papilloma, papillary urothelial neoplasm of low malignant potential (PUNLMP), and as Grade 1, Grade 2, and Grade 3 urothelial carcinoma. The biologic po
Accumulated allelic losses in the development of invasive urothelial cancer
β Scribed by Tomonori Habuchi; Osamu Ogawa; Yoshiyuki Kakehi; Keiji Ogura; Masahiro Koshiba; Shuji Hamazaki; Rei Takahashi; Taketoshi Sugiyama; Osamu Yoshida
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- French
- Weight
- 659 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0020-7136
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β¦ Synopsis
Abstract
To investigate the roles of allelic loss in the development of urothelial cancer, loss of heterozygosity was examined on 7 chromosomal arms in 49 cases of urothelial cancer of various grades and stages. Loss of heterozygosity was found on alleles in order of frequency as follows: 9q (21/38, 55%), 11p (20/44, 45%), 17p (18/42,43%), 13q (10/39,26%), 3p (8/41, 20%), 10q 2/29, 7%) and 1p (1/36, 3%). lnvasive (highβgrade or β₯pT2) tumors showed the loss of 17p (13/16,81%) and the loss of 13q (7/16, 44%) with significantly higher frequencies than nonβinvasive (grade 1β2 β€~p~TI ) tumors. Although the loss of 3p and the loss of 11p were also more frequently associated with the invasive phenotypes, the loss of 11p was detected in a considerable number (9 of 26,35%) of nonβinvasive tumors. Our results indicate that the loss of 11p might generally occur at an earlier stage before the loss of 3p, 13q or 17p in tumor progression. Since no correlation was found between the loss of 9q and the tumor grade or stage, this genetic alteration appears to be unrelated to invasiveness, and could be one of the initial events in tumorigenesis. Although accumulated allelic losses of 3p, 11p, 13q and 17p are considered to be involved in the development of the invasive type of urothelial cancers, these multiple genetic alterations may have already occurred in some pathologically nonβinvasive urothelial cancers. Furthermore, there appears to be some variation in the pattern of cumulative allelic loss.
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Forty-eight samples of primary non-small-cell lung cancer (NSCLC) and normal tissue from the same patients were analyzed for allelic deletions on chromosome I I p. Five polymorphic loci were assessed to determine the incidence of I Ip sequence deletions and to define hot-spots of deletions. Informat
DNA was prepared from tumour and normal tissue from 48 patients representing all common histological types of nonsmall-cell lung cancer. Using eight DNA probes, which detect nine restriction enzyme fragment length polymorphisms (RFLP) on chromosome 3, we established that among the 44 informative pat