Uchida H, Ando H, Maruyama K, Kobayashi H, Toda H, Ogawa H, Ozawa T, Matsuda Y, Sugimura H, Kanno T, Baba S
Department of Laboratory Medicine, Hamamatsu University School of Medicine.
Jpn J Cancer Res. 1998 Mar;89(3):299-306. doi: 10.1111/j.1349-7006.1998.tb00562.x.
Some mixed hyperplastic adenomatous polyps (MHAPs) contain dysplastic lesions or even carcinomas. These polyps are considered to be different from ordinary hyperplastic polyps and may have a preneoplastic potential. We investigated APC and K-ras mutations in MHAPs of the colon and rectum, and also in colorectal adenomas and hyperplastic polyps to identify molecular differences between MHAPs, adenomas and hyperplastic polyps, using direct sequencing of mutation cluster regions (MCR) in APC and K-ras. No APC mutations were identified in 12 MHAPs and 8 hyperplastic polyps, whereas 10 of 27 (37.0%) adenomas showed somatic mutations. K-ras mutations were identified in one of 12 (8.3%) MHAPs, one of 8 (12.5%) hyperplastic polyps, and 10 of 27 (37.0%) adenomas. p53 mutation was found in a carcinoma arising in an MHAP. Mutations other than APC mutations may play a role in the development of MHAPs.
一些混合性增生性腺瘤性息肉(MHAPs)含有发育异常病变甚至癌。这些息肉被认为与普通增生性息肉不同,可能具有癌前潜能。我们研究了结肠和直肠MHAPs以及结直肠腺瘤和增生性息肉中的APC和K-ras突变,通过对APC和K-ras中突变簇区域(MCR)进行直接测序,以确定MHAPs、腺瘤和增生性息肉之间的分子差异。在12个MHAPs和8个增生性息肉中未发现APC突变,而27个腺瘤中有10个(37.0%)出现体细胞突变。在12个MHAPs中的1个(8.3%)、8个增生性息肉中的1个(12.5%)以及27个腺瘤中的10个(37.0%)中发现了K-ras突变。在一个起源于MHAP的癌中发现了p53突变。除APC突变外的其他突变可能在MHAPs的发生发展中起作用。