Rigas B
Division of Digestive Diseases, New York Hospital--Cornell Medical Center, NY 10021.
J Clin Gastroenterol. 1990 Oct;12(5):494-9.
Abnormalities in oncogenes, which are broadly classified into viral and cellular oncogenes, and suppressor genes appear critical for the development of colon cancer. Cellular oncogenes contribute to malignant transformation when they become activated by point mutation, translocation, amplification, or loss of regulator sequences. The properties of the oncoproteins, the proteins encoded by oncogenes which are essential for carcinogenesis, are unclear. Suppressor genes normally suppress the tumorigenic phenotype by keeping the growth of cells in check; it is their inactivation that contributes to malignant transformation. Development of colon cancer appears to take place by stepwise accumulation of multiple genetic alterations during the progression from normal colon to adenoma and carcinoma. Activation of ras, an early event in this sequence, is found in 50% of colon cancers; overexpression of c-myc is found in approximately 80%. Inactivation of suppressor genes, which occurs during later stages, is noted in greater than 70% of tumors. A current model of colonic tumorigenesis is presented.
癌基因异常（大致分为病毒癌基因和细胞癌基因）以及抑癌基因异常似乎对结肠癌的发生发展至关重要。细胞癌基因在通过点突变、易位、扩增或调控序列缺失而被激活时，会促使恶性转化。癌蛋白（癌基因所编码的对致癌作用至关重要的蛋白质）的特性尚不清楚。抑癌基因通常通过控制细胞生长来抑制致瘤表型；正是它们的失活导致了恶性转化。从正常结肠发展到腺瘤和癌的过程中，结肠癌的发生似乎是通过多种基因改变的逐步积累而发生的。ras激活是这一过程中的早期事件，在50%的结肠癌中可以发现；约80%的结肠癌中可发现c-myc的过表达。抑癌基因失活发生在后期阶段，在超过70%的肿瘤中可以观察到。本文提出了一个当前的结肠肿瘤发生模型。
