Kane K
Department of Pathology, Good Samaritan Hospital and Health Center, Dayton, OH 45406.
Ann Clin Lab Sci. 1994 Jul-Aug;24(4):287-93.
Colorectal neoplasms begin as monoclonal cell populations, presumably arising from a single mutation or from a series of mutations in a single epithelial cell. Identification of the earliest mutation has been elusive. The resulting neoplastic clone is genetically unstable, perhaps owing to reduced methyl content of the deoxyribonucleic acid (DNA) molecules. Loss of DNA repair mechanisms may also be a factor. There are multiple genetic pathways to colorectal carcinoma (CRC). The multiplicity of mutations which are often associated with carcinogenesis suggests that the cancer cell is specifically adapted to its parasitic role. This is especially apparent when cancer cells become capable of invasion and metastasis. Early therapeutic experiments in vitro suggest that the carcinogenic process may be disrupted by correction of any one of the multiple genetic defects.
结直肠肿瘤起源于单克隆细胞群体，推测是由单个上皮细胞中的单个突变或一系列突变引起的。最早突变的鉴定一直难以捉摸。由此产生的肿瘤克隆在基因上不稳定，这可能是由于脱氧核糖核酸（DNA）分子的甲基含量降低所致。DNA修复机制的丧失也可能是一个因素。结直肠癌（CRC）有多种遗传途径。通常与致癌作用相关的多种突变表明癌细胞特别适应其寄生角色。当癌细胞能够侵袭和转移时，这一点尤为明显。早期的体外治疗实验表明，致癌过程可能会因纠正多个基因缺陷中的任何一个而被破坏。
