Allelic deletion at chromosome 9p21(p16) and 17p13(p53) in microdissected sporadic dysplastic nevus

被引:57
|
作者
Park, WS
Vortmeyer, AO
Pack, S
Duray, PH
Boni, R
Ali Guerami, A
Emmert-Buck, MR
Liotta, LA
Zhuang, ZP
机构
[1] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA
[2] Univ Zurich Hosp, Dept Dermatol, Zurich, Switzerland
基金
美国国家卫生研究院;
关键词
dysplastic nevus; chromosome; 9; 17; PCR; loss of heterozygosity;
D O I
10.1016/S0046-8177(98)90221-0
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
A critical area of chromosomal loss at region p16(9p21-22) and p53(17p13) has been implicated in the genesis of malignant melanoma. It is still unclear whether the genetic alterations can be detected in dysplastic nevus, a premalignant lesion of malignant melanoma. We have searched the frequency of p16 and p53 deletion in nine dysplastic nevi and 13 benign intradermal nevi with five microsatellite markers. Hemizygous deletion was detected in seven of nine (78%) dysplastic nevi at one or more loci for p16 and three of seven (43%) for p53, respectively. No loss of heterozygosity (LOH) was detected in any of the benign intradermal nevi. All three dysplastic nevi with LOH for p53 also showed LOH at p16. However, not all dysplastic nevi showing p16 deletion showed P53 gene deletion. Therefore, these data suggest that deletion of p16 may play an important role in the development of dysplastic nevus as an early event and that the changes may represent an early event in the development of malignant melanoma. This is a US government work. There are no restrictions on its use.
引用
收藏
页码:127 / 130
页数:4
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