Ha Tae-Won, Han Ki-Hwan, Son Dae-Gu, Kim Sang-Pyo, Kim Dae-Kwang
Department of Plastic and Reconstructive Surgery, Keimyung University School of Medicine, Daegu 700-712, Korea.
J Korean Med Sci. 2005 Apr;20(2):340-3. doi: 10.3346/jkms.2005.20.2.340.
Loss of heterozygosity (LOH) has been established as an important genetic mechanism giving rise to malignant neoplasia. The mechanism of LOH has been shown to cause basal cell carcinoma and malignant melanoma as well as other types of skin cancer. A few studies on LOH in sporadic keratoacanthomas have been reported. The purpose of this study was to investigate the significance of LOH in the pathogenesis of sporadic keratoacanthomas developed in 10 Korean patients. The presents of LOH at 7 microsatellite markers (D2S286, D3S1317, D5S346, D9S160, D9S171, D10S185, and D17S261) were evaluated in sporadic keratoacanthomas. LOH was found in only 1 of 10 cases at D10S185. The low frequency of LOH detected in this study suggests that LOH may not be significant in the induction of sporadic keratoacanthomas.
杂合性缺失(LOH)已被确认为引发恶性肿瘤的一种重要遗传机制。LOH机制已被证明可导致基底细胞癌、恶性黑色素瘤以及其他类型的皮肤癌。已有一些关于散发性角化棘皮瘤中LOH的研究报道。本研究的目的是调查10例韩国患者发生的散发性角化棘皮瘤发病机制中LOH的意义。在散发性角化棘皮瘤中评估了7个微卫星标记(D2S286、D3S1317、D5S346、D9S160、D9S171、D10S185和D17S261)处的LOH情况。在10例病例中仅1例在D10S185处发现LOH。本研究中检测到的LOH低频率表明,LOH在散发性角化棘皮瘤的诱发中可能并不重要。