NONINVOLVEMENT OF RAS MUTATIONS IN FLAT COLORECTAL ADENOMAS AND CARCINOMAS
NONINVOLVEMENT OF RAS MUTATIONS IN FLAT COLORECTAL ADENOMAS AND CARCINOMAS
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DOI：
10.1002/ijc.2910570110
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发表时间：
1994-04-01
影响因子：
6.4
通讯作者：
MAEDA, S
中科院分区：
文献类型：
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作者：
FUJIMORI, T;SATONAKA, K;MAEDA, S
Ras基因突变在结直肠肿瘤发展过程中相对较早发生，并且在40-50%的恶性结直肠肿瘤中观察到。内窥镜技术的进步使人们有可能发现小，平坦的结直肠肿瘤，不能通过标准检查发现。为了确定ras基因突变是否也参与了小而平坦的结直肠肿瘤的发生，我们检测了ras点突变的34例小息肉或平坦隆起的结直肠肿瘤（32腺瘤，2癌）和26例小而平坦的结直肠肿瘤（13腺瘤，13癌）通过聚合酶链反应（PCR）和斑点杂交。Ras基因点突变在前一种类型的34个肿瘤中的16个（47%）中观察到，而在后一种类型的26个肿瘤中没有发现，即使在扁平肿瘤中异型增生程度严重。我们的研究结果表明，息肉样和扁平结直肠癌可能存在不同的肿瘤进展的遗传途径。(C)1994 Wiley-Liss，Inc.
Ras gene mutations occur relatively early during colorectal tumor development and have been observed in 40-50% of malignant colorectal tumors. Advances in endoscopic techniques have made it possible to detect small, flat colorectal tumors that could not be detected by standard examinations. To determine whether ras gene mutations are also involved in the genesis of small, flat colorectal tumors, we examined ras point mutations in 34 cases of small polypoid or flat elevated colorectal tumors (32 adenomas, 2 carcinomas) and in 26 cases of small, flat colorectal tumors (13 adenomas, 13 carcinomas) by means of the polymerase chain reaction (PCR) and dot-blot hybridization. Ras gene point mutations were observed in 16 of the 34 tumors of the former type (47%), but in none of the 26 tumors of the latter type, even though the grade of dysplasia was severe in the flat tumors. Our results suggest that different genetic pathways for tumor progression may exist for polypoid and for flat colorectal carcinomas. (C) 1994 Wiley-Liss, Inc.