脑原发性恶性淋巴瘤:通过PCR-SSCP分析和免疫组织化学证明p53基因突变。

H Koga, S Zhang, T Ichikawa, K Washiyama, T Kuroiwa, R Tanaka, T Kumanishi
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引用次数: 0

摘要

应用PCR-SSCP和免疫组化方法,对5例原发性脑恶性淋巴瘤(弥漫性大细胞型)的p53抑癌基因突变进行了检测。经PCR-SSCP及核苷酸分析,5例患者中2例出现p53基因突变。一个病例的突变是错义G: C-T:密码子176处的翻转(TGC-TTC;Cys-Phe)位于高度保守的结构域,并毗邻先前提出的各种肿瘤的热点密码子(密码子175)。在本病例中也显示了P53的免疫反应性。另一个病例的突变是密码子52处的无义G:C-A:T转移(TGG-TGA;色氨酸停止密码子)导致截断的p53肽。因此,这些突变实际上可能导致了p53蛋白结构和功能的严重改变。这些发现提示p53基因突变与原发性脑恶性淋巴瘤的肿瘤发生有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Primary malignant lymphoma of the brain: demonstration of the p53 gene mutations by PCR-SSCP analysis and immunohistochemistry.

Using PCR-SSCP and immunohistochemical analyses, mutations of the p53 tumor suppressor gene were examined in 5 cases of primary malignant lymphoma of the brain (diffuse large cell type). By PCR-SSCP and nucleotide analyses, p53 gene mutations were seen in 2 of the 5 cases. The mutation in one case was a missense G: C-T:A transversion at codon 176 (TGC-TTC; Cys-Phe) which was located in the highly conserved domains and adjoined a previously proposed hot spot codon (codon 175) in various tumors. p53 immunoreactivity was also shown in this case. The mutation in another case was a nonsense G:C-A:T transition at codon 52 (TGG-TGA; Trp-stop codon) leading to a truncated p53 peptide. Thus, these mutations may have actually given rise to serious structural and functional alterations of the p53 protein. These findings suggested that the p53 gene mutation was related with oncogenesis in the primary malignant lymphoma of the brain.

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