Waliszewski P
Department of Clinical Pathomorphology, School of Medicine, Poznań.
Patol Pol. 1992;43(3):73-8.
Carcinogenesis in human large intestine is a result of multiple, heterogeneous and random genetic changes. Deletion of tumor suppressor genes and activation of oncogenes appear to be important molecular events. These compromise the loss of chromosomes 5, 17, 18 or functional inactivation of FAP, p53 and DCC genes. Activation of Ki-ras and c-myc oncogenes seems to be crucial for both cell immortalization and morphology modification. Identification of genes involved in this process enables both a screening and a new classification. Also it is an important step towards a gene therapy.
人类大肠中的致癌作用是多种、异质性和随机性基因变化的结果。肿瘤抑制基因的缺失和癌基因的激活似乎是重要的分子事件。这些涉及5号、17号、18号染色体的缺失或FAP、p53和DCC基因的功能失活。Ki-ras和c-myc癌基因的激活对于细胞永生化和形态改变似乎都至关重要。鉴定参与这一过程的基因有助于进行筛查和新的分类。这也是迈向基因治疗的重要一步。