In a loss of heterozygosity analysis of 3p, we examined 44 sporadic cases of renal cell carcinoma (RCC) and matched normal tissue with 18 markers distributed over the whole p-arm. The majority of these markers clustered in three regions that have been suggested t o be involved in the development of
A comprehensive analysis of loss of heterozygosity caused by hemizygous deletions in renal cell carcinoma using a subtraction library
✍ Scribed by Naoya Hatano; Naoko S. Nishikawa; Cathal McElgunn; Shubhashish Sarkar; Kazuo Ozawa; Yasuhiko Shibanaka; Motowo Nakajima; Kazuo Gohiji; Ryoiti Kiyama
- Book ID
- 102500755
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 189 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.1051
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✦ Synopsis
Abstract
Several new loci were identified by a comprehensive analysis of loss of heterozygosity (LOH) using a subtraction library between matched normal and renal cell carcinoma (RCC) tissues. A total of 187 clones from the library, with a complexity of 1×10^4^, were mapped, and 44 clusters of the mapped loci were subjected to LOH analysis using microsatellite markers. A total of 27 loci, which exhibited frequencies of LOH of at least 10% among 44 tumors, mostly clear‐cell RCC, included several loci that were reported previously, such as, the von Hippel‐Lindau gene, adenomatous polyposis coli, and interferon regulatory factor‐1, as well as new loci, at 5q32‐q34, 6q21‐q22, 8p12, and others. These loci exhibited LOH among 11.8–93.8% of tumors, and most, if not all, were derived from the sites of hemizyous deletions. The minimum regions of LOH of chromosomes 5, 6, and 8 were 9.0, 10.3, and 0.775 Mb, respectively. The average distance between the cloned fragments on the chromosomes was 2.2 Mb in 187 clones, indicating that the minimum LOH size expected from this subtraction analysis was roughly 50 kb. Therefore, the strategy described here provides comprehensive analysis of LOH sites, which were mostly caused by hemizygous deletions. © 2001 Wiley‐Liss, Inc.
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