Sakurai S, Sano T, Maeshima A, Kashiwabara K, Oyama T, Fukuda T, Nakajima T
Second Department of Pathology, Gunma University School of Medicine, Gunma, Japan.
Virchows Arch. 1995;427(2):119-24. doi: 10.1007/BF00196515.
With the aim of detecting the timing of p53 and Ki-ras gene alterations in the gastric adenoma-carcinoma sequence, 19 early gastric adenocarcinomas arising from adenomas were studied. Immunohistochemically, 5 adenocarcinomas were positive for p53; 3 focally and 2 diffusely. The p53 point mutations were detected in a focal area with p53 immunoreactivity in 2 of the 5 p53-positive adenocarcinomas. This indicated that p53 point mutations may play a less crucial part in malignant conversion of adenoma to adenocarcinoma in the stomach than in the colon. No Ki-ras gene mutations at codons 12 and 13 were detected in any lesion. These results suggest that the adenoma-carcinoma sequence in the stomach has a different mechanism from that in the colon.
为了检测胃腺瘤-癌序列中p53和Ki-ras基因改变的时间,对19例起源于腺瘤的早期胃腺癌进行了研究。免疫组织化学检测发现,5例腺癌p53呈阳性;3例为局灶性阳性,2例为弥漫性阳性。在5例p53阳性腺癌中的2例中,在p53免疫反应阳性的局灶区域检测到p53点突变。这表明,与结肠相比,p53点突变在胃腺瘤向腺癌的恶性转化中可能起的作用较小。在任何病变中均未检测到第12和13密码子的Ki-ras基因突变。这些结果提示,胃的腺瘤-癌序列与结肠的腺瘤-癌序列具有不同的机制。