Kim E C, Lance P
Department of Medicine, State University of New York at Buffalo, USA.
Gastroenterol Clin North Am. 1997 Mar;26(1):1-17. doi: 10.1016/s0889-8553(05)70280-6.
Autosomal dominant, familial forms of colorectal adenocarcinoma are recognized, but more than 90% of cases are sporadic. Most familial and sporadic cases arise through malignant transformation of benign adenomas in a process known as the adenoma-to-carcinoma sequence. Adenomas are classified histologically as tubular, tubulovillous, or villous. As a neoplasm, adenomas all manifest mild, moderate, or severe dysplasia. The majority (> 90%) of adenomas are small (< 1 cm in diameter) and do not progress. Risk factors for carcinomatous progression include the presence of multiple adenomas, size greater than or equal to 1 cm, and villous histology or severe dysplasia in adenomas of any size. The adenoma-to-carcinoma sequence advances through the accumulation of lesions involving multiple genes. It appears that similar molecular genetic mechanisms are involved in familial and sporadic forms of colorectal neoplasia.
常染色体显性遗传的家族性结直肠癌已得到确认，但超过90%的病例为散发性。大多数家族性和散发性病例是通过良性腺瘤在一个被称为腺瘤-癌序列的过程中发生恶性转化而产生的。腺瘤在组织学上分为管状、管状绒毛状或绒毛状。作为一种肿瘤，腺瘤均表现为轻度、中度或重度发育异常。大多数（>90%）腺瘤较小（直径<1 cm）且不会进展。癌进展的危险因素包括多个腺瘤的存在、大小大于或等于1 cm，以及任何大小腺瘤的绒毛状组织学或重度发育异常。腺瘤-癌序列通过涉及多个基因的病变积累而进展。似乎相似的分子遗传机制参与了结直肠肿瘤的家族性和散发性形式。
