Kok Sang-Heng, Lee Jang-Jaer, Hsu Hey-Chi, Chiang Chun-Pin, Kuo Ying-Shiung, Kuo Mark Yen-Ping
School of Dentistry, College of Medicine, National Taiwan University, Taipei, Taiwan.
J Oral Pathol Med. 2002 Aug;31(7):395-401. doi: 10.1034/j.1600-0714.2002.00118.x.
Adenomatous polyposis coli (APC) gene mutations have been demonstrated not only in colorectal tumors but also in a variety of human cancers.
To elucidate the possible roles of APC gene mutations in oral squamous cell carcinomas (OSCCs), we examined 40 untreated human primary OSCCs using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and DNA sequencing assays.
By screening nearly one-half of the coding region (codons 279-1673, including the MCR) of the APC gene, five missense mutations and a 1-base pair deletion were detected in five (12.5%) tumors, resulting in five amino-acid substitutions or a truncation of the APC protein. All patients with APC mutations were both areca quid chewers and tobacco smokers (P = 0.049).
These results suggest that APC mutations may also contribute to the carcinogenesis of at least some OSCCs in Taiwan, especially for the users of areca quid and tobacco.
已证实腺瘤性息肉病 coli(APC)基因突变不仅存在于结直肠肿瘤中,也存在于多种人类癌症中。
为阐明 APC 基因突变在口腔鳞状细胞癌(OSCC)中的可能作用,我们使用聚合酶链反应-单链构象多态性(PCR-SSCP)和 DNA 测序分析检测了 40 例未经治疗的人类原发性 OSCC。
通过筛查 APC 基因近一半的编码区(密码子 279 - 1673,包括 MCR),在 5 个(12.5%)肿瘤中检测到 5 个错义突变和 1 个 1 碱基对缺失,导致 APC 蛋白发生 5 个氨基酸替换或截短。所有 APC 突变患者均既嚼槟榔又吸烟(P = 0.049)。
这些结果表明,APC 突变可能也促成了台湾至少部分 OSCC 的致癌过程,尤其是对于槟榔和烟草使用者。