p53 mutation and protein overexpression in the early stages of esophageal tumorigenesis utilizing endoscopically obtained biopsy specimens.
p53 mutation and protein overexpression in the early stages of esophageal tumorigenesis utilizing endoscopically obtained biopsy specimens.
复制标题
利用内窥镜获得的活检标本研究食管肿瘤发生早期的 p53 突变和蛋白质过度表达。
DOI：
10.3892/ijo.10.4.683
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发表时间：
1997
影响因子：
5.2
通讯作者：
K. Ishizaki
中科院分区：
文献类型：
--
作者：
G. Kim;H. Yamabe;Y. Imadashirakata;S. Ueda;M. Sakai;M. Okuma;K. Ishizaki
目前尚不清楚p53在食管癌发生早期的异常是否会导致肿瘤生长时的克隆性扩张。在这项研究中，我们分析了86例食管内镜活检标本的p53异常的PCR-SSCP和免疫组化。27例轻度发育不良标本中有11例（39%）显示p53突变。6例中度或轻度发育不良的内镜检查（平均73周），并继续表现出相同的p53突变，但没有一个显示出明显的肿瘤生长和上皮下上皮浸润。提示p53基因突变在食管癌发生的早期即已发生，并促进细胞增殖，但与食管癌恶性表型无直接关系。
It is unclear whether p53 abnormality in the early esophageal tumorigenesis causes clonal expansion with tumor growth. In this study, we analyzed p53 abnormalities by PCR-SSCP and immunohistochemistry in 86 esophageal endoscopic biopsy specimens. Eleven of 27 specimens (39%) of mild dysplasias showed p53 mutations. Six moderate or mild dysplasias were followed by endoscopy (average 73 weeks) and continually exhibited the same p53 mutation, but none of them showed apparent tumor growth and subepithelial epithelial invasion. These results suggest that p53 mutations occur very early in the esophageal tumorigenesis and contribute to cell proliferation, but cannot be related with malignant phenotype directly.