Shirasawa S, Yanagawa Y, Sasazuki T
Department of Genetics, Kyushu University, Fukuoka, Japan.
Gan To Kagaku Ryoho. 1991 Jan;18(1):14-21.
The inherited cancer-inducing disease familial polyposis coli (FPC) provides an excellent model not only for studying tumor progression in colorectal cancer but also for elucidating molecular mechanisms in general oncogenesis. This paper reviewed recent remarkable progresses of molecular mechanisms in colorectal tumorigenesis. This is concerned with the various kinds of genetic alterations that accumulate in the development from normal mucosa to adenoma, and then to adenocarcinoma in comparison with FPC and sporadic cases. This review included also information on the localization of FPC major gene. These observations indicate that in cases of colorectal tumorigenesis several genetic alterations may be involved, including activation of K-ras gene, deregulated expression of c-myc gene or c-fos gene and inactivation of tumor suppressor genes such as p53 and DCC genes, as well as the loss of heterozygosity. The observation suggest that adenomas will have undergone several gene or chromosome mutations before reaching to the fully malignant state. Therefore, DNA diagnosis for colorectal tumors in the clinical level may contribute to more accurate prognosis and better results for further therapy.
遗传性致癌疾病家族性结肠息肉病（FPC）不仅为研究结直肠癌的肿瘤进展提供了一个极佳模型，也为阐明一般肿瘤发生的分子机制提供了模型。本文综述了结直肠癌发生分子机制的近期显著进展。这涉及从正常黏膜发展到腺瘤，再到腺癌过程中积累的各种基因改变，并与FPC及散发病例进行了比较。本综述还包括FPC主要基因定位的信息。这些观察结果表明，在结直肠癌发生过程中可能涉及多种基因改变，包括K-ras基因的激活、c-myc基因或c-fos基因的表达失调以及肿瘤抑制基因如p53和DCC基因的失活，还有杂合性缺失。这些观察结果提示，腺瘤在发展到完全恶性状态之前可能已经经历了多个基因或染色体突变。因此，临床水平上对结直肠癌的DNA诊断可能有助于更准确的预后评估，并为进一步治疗带来更好的结果。
