Pancreatic cancer has one of the poorest prognoses among malignant diseases. To understand its molecular mechanisms, we studied allelic losses on the long arm of chromosome 6. Using 55 paired DNAs of tumors and their corresponding normal tissues and 30 microsatellite markers that spanned the entire
Genetic alterations in localized prostate cancer: Identification of a common region of deletion on chromosome arm 18q
✍ Scribed by Alain Latil; Jean-Christophe Baron; Olivier Cussenot; Georges Fournier; Thierry Soussi; Laurent Boccon-Gibod; Alain Le Duc; Jacques Rouëssé; Rosette Lidereau
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 964 KB
- Volume
- 11
- Category
- Article
- ISSN
- 1045-2257
No coin nor oath required. For personal study only.
✦ Synopsis
Accumulation of mutations in oncogenes and tumor suppressor genes transforms a normal cell into a malignant cell by allowing it to escape from normal control of growth. In prostate tumorigenesis, the current model envisages specific mutations of the TP53 tumor suppressor gene and loss of loci, detected by loss of heterozygosity (LOH), on chromosome arms 8p, IOq, 16q, and I8q. In order to determine if alterations frequently found in other adenocarcinomas (breast, ovarian, gastric, colorectal), including losses of genetic material from chromosome arms I p, 3p, 7q, 8p, I I p, I7p, I7q, and I8q, are also involved in prostate cancer, we examined 20 localized early-stage prostate tumors. We detected no mutations of the TP53 gene. Allelic losses were found from 7q (33%), 8p (50%), IOq (20%), and 18q (33%). Furthermore, as the first step toward isolating tumor suppressor genes on I8q, we used six polymorphic markers and identified a small common deleted region between the chromosome I8 centromere and the D 18s I9 locus. Genes Chromosom Cancer I I; I 19-125 (1994). 0 I994 Wiley-Liss, Inc.
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