Loss of Heterozygosity at VHL, FHIT, and p16 Loci in Nonpapillary Renal Cell Carcinoma.
- Author:
Won Sang PARK
;
Seung Myung DONG
;
Yong Hyun CHO
;
Tae Gon HWANG
;
Su Young KIM
;
Min Sun SHIN
;
Jae Ho PI
;
Suk Hyung LEE
;
Nam Jin YOO
;
Jung Young LEE
- Publication Type:Original Article
- Keywords:
Renal cell carcinoma;
LOH;
VHL;
FHIT;
p16
- MeSH:
Carcinogenesis;
Carcinoma, Renal Cell*;
Humans;
Loss of Heterozygosity*;
Microsatellite Repeats;
Paraffin
- From:Korean Journal of Pathology
1999;33(1):8-14
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The objectives of this study were to characterize the alterations of 3p and 9p in sporadic renal cell carcinomas (RCC) and to assess the relationship between the clinical stages or tumor size and the alteration of these chromosomes. Thirty eight archival, paraffin embedded tissue sections from 38 patients with RCC were analyzed for loss of heterozygosity (LOH) at 3p and 9p with 11 microsatellite markers. LOH was detected in 81.6% (31/38) and 37.8% (14/37) at 3p and 9p, respectively. The frequencies of LOH at VHL and FHIT locus were 75.6% and 72.2%, respectively. Twelve cases out of 38 showed LOH at both 9p21 and 3p. The loss of 3p in the samples tested was not related to clinical stages and tumor size, but that of 9p21 was significantly associated with advanced stage and larger tumor size. These results support that 3p deletion, including VHL and FHIT gene, play a critical role in the tumorigenesis of sporadic RCC, especially at early stage, and that 9p21 may contribute to the progression of sporadic RCC.
