Kuo M Y, Huang J S, Hsu H C, Chiang C P, Kok S H, Kuo Y S, Hong C Y
School of Dentistry, College of Medicine, National Taiwan University, Taipei, Taiwan.
J Oral Pathol Med. 1999 May;28(5):221-5. doi: 10.1111/j.1600-0714.1999.tb02028.x.
Mutations in the conserved regions (exons 5-9) of the p53 gene were investigated in 37 untreated human primary oral squamous cell carcinomas (SCCs) using polymerase chain reaction-single strand conformation polymorphism and DNA sequencing analyses. P53 mutations were detected in 2 of 37 (5.4%) oral SCC cases. One tumor sample (case 23) showed a mis-sense point mutation at codon 177, changing CCC to CTC, which resulted in a substitution of proline to leucine in the p53 protein. The other tumor (case 33) had a point mutation at codon 266, changing GGA to AGA and causing a substitution of glycine to arginine in the p53 protein. These two patients with p53 mutations did not have an areca quid chewing habit. These results suggest that mutations in the p53 gene may not play a role in the pathogenesis of human oral SCCs in Taiwan. Recently, we have shown that positive p53 staining was observed in 47 of 81 (58%) cases of oral SCC. The discrepancies between positive p53 protein staining and the low prevalence of p53 mutation in oral SCCs indicate that other mechanism(s) are involved in p53 overexpression.
利用聚合酶链反应-单链构象多态性分析和DNA测序分析，对37例未经治疗的人类原发性口腔鳞状细胞癌（SCC）的p53基因保守区域（外显子5-9）的突变情况进行了研究。在37例口腔SCC病例中有2例（5.4%）检测到p53突变。一个肿瘤样本（病例23）在密码子177处出现错义点突变，由CCC变为CTC，导致p53蛋白中的脯氨酸被亮氨酸取代。另一个肿瘤（病例33）在密码子266处有一个点突变，由GGA变为AGA，导致p53蛋白中的甘氨酸被精氨酸取代。这两名有p53突变的患者没有嚼食槟榔的习惯。这些结果表明，p53基因的突变可能在台湾地区人类口腔SCC的发病机制中不起作用。最近，我们发现81例口腔SCC中有47例（58%）p53染色呈阳性。口腔SCC中p53蛋白阳性染色与p53突变低发生率之间的差异表明，p53过表达涉及其他机制。
