Cummings O W
Department of Pathology, Indiana University School of Medicine, Indianapolis, USA.
Semin Gastrointest Dis. 2000 Oct;11(4):229-37.
The adenoma-carcinoma sequence postulates that colorectal carcinomas arise from precursor lesions, called adenomas. All adenomas contain dysplastic epithelium that arises from mutations in either the adenomatous polyposis coli gene or DNA mismatch repair genes. The earliest lesion detected with dysplasia is the aberrant crypt focus. Over time, as this lesion acquires additional mutations, it evolves into a classic adenomatous polyp. Adenomatous polyps are classified as tubular, tubulovillous, or villous. Generally, as polyps increase in size, the degree of dysplasia worsens, the villous component increases, the number of genetic abnormalities increases, and the likelihood of harboring invasive carcinoma increases. Carcinomas associated with DNA mismatch repair mutations are more likely to be poorly differentiated and incite a host lymphocytic response. These tumors seem to have a better prognosis, stage for stage, than typical colorectal carcinomas.
腺瘤-癌序列假说认为，结直肠癌起源于称为腺瘤的前驱病变。所有腺瘤都含有发育异常的上皮，其由腺瘤性息肉病 coli 基因或 DNA 错配修复基因的突变产生。最早检测到发育异常的病变是异常隐窝灶。随着时间的推移，随着该病变获得更多突变，它会演变成典型的腺瘤性息肉。腺瘤性息肉分为管状、管状绒毛状或绒毛状。一般来说，随着息肉大小增加，发育异常程度加重，绒毛成分增加，基因异常数量增加，发生浸润性癌的可能性增加。与 DNA 错配修复突变相关的癌更可能分化不良并引发宿主淋巴细胞反应。这些肿瘤似乎在各分期中比典型结直肠癌预后更好。
