Yamagata S, Muto T, Uchida Y, Masaki T, Sawada T, Tsuno N, Hirooka T
First Department of Surgery, University of Tokyo.
Jpn J Cancer Res. 1994 Feb;85(2):147-51. doi: 10.1111/j.1349-7006.1994.tb02075.x.
In order to clarify genetic changes in flat adenomas, K-ras codon 12 point mutations were examined in 56 flat adenomas, 81 polypoid adenomas and 42 cancers of colon and rectum. The mutation frequency in flat adenomas was 23% (13/56), significantly lower than that in polypoid adenomas (67%: 54/81) and cancers (76%: 32/42). Even mildly dysplastic adenomas or small (less than 5 mm) adenomas showed higher mutation incidence in polypoid type (62%, 57%) than in flat type (23%, 19%). Among flat adenomas, flat elevated lesions exhibited relatively higher mutation frequency than completely flat or depressed ones. As for cancers, 14 tumors (33%) contained mutations only in a minor tumor cell population, indicating that these mutations occur at a late stage of tumorigenesis. These results suggest that the adenoma-carcinoma sequence through flat adenomas may be different from that through polypoid adenomas, and genetic changes may be heterogeneous in colorectal carcinogenesis.
为了阐明扁平腺瘤的基因变化,我们检测了56例扁平腺瘤、81例息肉状腺瘤以及42例结肠直肠癌中的K-ras密码子12点突变情况。扁平腺瘤的突变频率为23%(13/56),显著低于息肉状腺瘤(67%:54/81)和癌(76%:32/42)。即使是轻度发育异常的腺瘤或小(小于5mm)腺瘤,息肉状类型的突变发生率(62%,57%)也高于扁平类型(23%,19%)。在扁平腺瘤中,扁平隆起性病变的突变频率相对高于完全扁平或凹陷性病变。至于癌,14个肿瘤(33%)仅在少数肿瘤细胞群体中存在突变,这表明这些突变发生在肿瘤发生的晚期。这些结果提示,通过扁平腺瘤的腺瘤-癌序列可能不同于通过息肉状腺瘤的序列,并且在结直肠癌发生过程中基因变化可能是异质性的。