Largey J S, Meltzer S J, Sauk J J, Hebert C A, Archibald D W
Department of Medicine (Gastroenterology Division), University of Maryland at Baltimore.
Oral Surg Oral Med Oral Pathol. 1994 Mar;77(3):260-3. doi: 10.1016/0030-4220(94)90295-x.
The tumor suppressor gene adenomatous polyposis coli has been shown to be altered in colon and esophageal cancers. Because of similar causes of oral and esophageal cancers, we investigated allelic deletion of the adenomatous polyposis coli gene in oral cancers by examining tumor cells of persons normally heterozygous at a polymorphic restriction site in adenomatous polyposis coli. Deoxyribonucleic acid was extracted from 20 formalin-fixed microdissected sections and one fresh specimen of oral squamous cell carcinomas and amplified with the use of the polymerase chain reaction. The amplified deoxyribonucleic acid was digested with Rsa I, subjected to polyacrylamide gel electrophoresis, and examined for loss of heterozygosity in adenomatous polyposis coli alleles. Samples from nine persons were homozygous for the adenomatous polyposis coli restriction site in both tumor and normal tissues and thus were uninformative. Three of the 12 samples from heterozygous persons showed loss of one adenomatous polyposis coli allele in tumor tissues. The loss of an adenomatous polyposis coli gene allele in 25% of the carcinomas examined suggests that inactivation of adenomatous polyposis coli or another neighboring gene on chromosome 5q may be involved in carcinogenesis in the oral cavity.
肿瘤抑制基因腺瘤性息肉病基因已被证实在结肠癌和食管癌中发生改变。由于口腔癌和食管癌的病因相似,我们通过检测腺瘤性息肉病基因多态性限制性位点通常为杂合子的人群的肿瘤细胞,研究了口腔癌中腺瘤性息肉病基因的等位基因缺失情况。从20个福尔马林固定的显微切割切片以及1个口腔鳞状细胞癌新鲜标本中提取脱氧核糖核酸,并使用聚合酶链反应进行扩增。扩增后的脱氧核糖核酸用Rsa I酶切,进行聚丙烯酰胺凝胶电泳,并检测腺瘤性息肉病基因等位基因的杂合性缺失。9个人的样本在肿瘤组织和正常组织中腺瘤性息肉病基因限制性位点均为纯合子,因此无信息价值。来自杂合子人群的12个样本中有3个在肿瘤组织中显示一个腺瘤性息肉病基因等位基因缺失。在所检测的25%的癌中腺瘤性息肉病基因等位基因缺失,这表明腺瘤性息肉病基因或5号染色体上另一个相邻基因的失活可能参与口腔癌的发生。