Ahnen D J
Department of Medicine, University of Colorado School of Medicine, Denver.
West J Med. 1991 Jun;154(6):700-5.
Strikingly rapid advances in the identification of genetic events that are important in colonic carcinogenesis have been made in the past several years. Specific inherited (adenomatous polyposis coli gene) and acquired (ras gene point mutations; c-myc gene amplification; allelic deletion at specific sites on chromosomes 5, 17, and 18) genetic abnormalities appear to be capable of mediating steps in the progression from normal to malignant colonic mucosa. Understanding these genetic factors and how they influence cellular function will have a profound effect on medical practice. High-risk populations will be (and are being) identified by genetic markers, thus allowing prevention and screening to be more precisely targeted to the population at risk; intervention strategies will be designed on the basis of the known cellular defects of neoplastic colonic mucosa; and new molecular preventive and therapeutic approaches can be developed.
在过去几年中,在确定对结肠癌发生发展至关重要的遗传事件方面取得了惊人的快速进展。特定的遗传性(腺瘤性息肉病 coli 基因)和获得性(ras 基因点突变;c-myc 基因扩增;染色体 5、17 和 18 上特定位点的等位基因缺失)遗传异常似乎能够介导从正常结肠黏膜到恶性结肠黏膜进展过程中的各个步骤。了解这些遗传因素及其如何影响细胞功能将对医学实践产生深远影响。高危人群将通过遗传标记被识别出来(并且正在被识别),从而使预防和筛查能够更精准地针对高危人群;干预策略将基于已知的肿瘤性结肠黏膜细胞缺陷来设计;并且可以开发新的分子预防和治疗方法。