Park W S, Vortmeyer A O, Pack S, Duray P H, Böni R, Guerami A A, Emmert-Buck M R, Liotta L A, Zhuang Z
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Hum Pathol. 1998 Feb;29(2):127-30. doi: 10.1016/s0046-8177(98)90221-0.
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.
9号染色体短臂16区（9p21 - 22）和17号染色体短臂13区（17p13）的关键染色体缺失区域与恶性黑色素瘤的发生有关。目前仍不清楚在发育异常痣（恶性黑色素瘤的一种癌前病变）中是否能检测到基因改变。我们用五个微卫星标记物检测了9个发育异常痣和13个良性真皮内痣中p16和p53基因缺失的频率。在9个发育异常痣中，分别有7个（78%）在一个或多个p16位点检测到半合子缺失，7个中有3个（43%）在p53位点检测到半合子缺失。在任何良性真皮内痣中均未检测到杂合性缺失（LOH）。所有3个p53基因发生杂合性缺失的发育异常痣在p16位点也显示杂合性缺失。然而，并非所有显示p16缺失的发育异常痣都显示p53基因缺失。因此，这些数据表明，p16缺失可能在发育异常痣的发生发展中作为早期事件起重要作用，且这些改变可能代表恶性黑色素瘤发生发展的早期事件。
