Deschner E E
Pathol Annu. 1983;18 Pt 1:205-19.
Adenoma formation in the colon has been shown to be initiated by an alteration in the genetic make-up which controls the repopulation of the mucosa. This defect is recognized primarily by an upward displacement of the major zone of DNA synthesis within one or a few crypts. Progression to a microadenoma involves an elevation of cell proliferation within these glands and may be hastened by mucosal responses to environmental and dietary factors which enhance cell turnover. The high proliferative activity of epithelial cells within these select crypts allows the unmasking of the neoplastic genotype and the expansion of these cells with a proliferative advantage. Continued rapid cell proliferation within the adenoma either indigenous to the excrescence or fueled additionally by luminal conditions may contribute to the evolution of a malignant genotype, the establishment of a severely dysplastic clone and ultimately to the production of invasive colon cancer.
结肠腺瘤的形成已被证明是由控制黏膜再增殖的基因组成改变引发的。这种缺陷主要通过一个或几个隐窝内DNA合成主要区域的向上移位来识别。进展为微腺瘤涉及这些腺体中细胞增殖的增加，并且可能因黏膜对增强细胞更新的环境和饮食因素的反应而加速。这些特定隐窝内上皮细胞的高增殖活性使得肿瘤基因型得以暴露，并且具有增殖优势的这些细胞得以扩增。腺瘤内持续快速的细胞增殖，无论是赘生物本身固有的，还是由管腔条件额外促进的，都可能导致恶性基因型的演变、严重发育异常克隆的形成，并最终导致侵袭性结肠癌的产生。
