Burmer G C, Levine D S, Kulander B G, Haggitt R C, Rubin C E, Rabinovitch P S
Department of Pathology, University of Washington School of Medicine, Seattle, Washington.
Gastroenterology. 1990 Aug;99(2):416-20. doi: 10.1016/0016-5085(90)91024-z.
Mutations in the first exon of the c-Ki-ras protooncogene were analyzed in carcinomas and dysplasias from patients with sporadic colon cancer and chronic ulcerative colitis by a combination of histological enrichment, cell sorting, polymerase catalyzed chain reaction, and direct sequencing. In contrast to sporadic colon carcinomas, where 52% (11 of 21) contained mutations in codon 12, only 1 of 28 samples of ulcerative colitis associated carcinoma or dysplasia contained a c-Ki-ras mutation, despite the presence of aneuploid cell populations. These results suggest that a different genetic pathway for tumor progression may exist between sporadic colon carcinoma and carcinomas arising in chronic ulcerative colitis.
通过组织学富集、细胞分选、聚合酶催化链反应和直接测序相结合的方法，对散发性结肠癌和慢性溃疡性结肠炎患者的癌组织及发育异常组织中c-Ki-ras原癌基因第一外显子的突变情况进行了分析。与散发性结肠癌不同，散发性结肠癌中有52%（21例中的11例）在密码子12处存在突变，而溃疡性结肠炎相关癌或发育异常的28个样本中只有1个含有c-Ki-ras突变，尽管存在非整倍体细胞群。这些结果表明，散发性结肠癌和慢性溃疡性结肠炎相关癌的肿瘤进展可能存在不同的遗传途径。
