LACK OF ALLELIC DELETION AND POINT MUTATION AS MECHANISMS OF P53 ACTIVATION IN HUMAN-MALIGNANT MELANOMA
LACK OF ALLELIC DELETION AND POINT MUTATION AS MECHANISMS OF P53 ACTIVATION IN HUMAN-MALIGNANT MELANOMA
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DOI：
10.1002/ijc.2910550407
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发表时间：
1993-10-21
影响因子：
6.4
通讯作者：
BARNHILL, RL
中科院分区：
文献类型：
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作者：
CASTRESANA, JS;RUBIO, MP;BARNHILL, RL
为了研究 p53 肿瘤抑制基因在人类黑色素瘤发展中的作用，通过聚合酶链反应/限制性片段长度多态性 (PCR/RFLP) 分析，在 46 例黑色素瘤中研究了 p53 杂合性缺失 (LOH)，并通过 聚合酶链反应/单链构象多态性（PCR/SSCP）分析。研究中使用了冷冻肿瘤和石蜡样本。我们无法在 12 个 BstUI 信息病例中检测到任何等位基因丢失，也无法检测到 p53 基因外显子 5 至 8 中的任何单一突变。我们的结果与 DNA 水平上的其他发现一起表明，p53 基因似乎并不普遍参与黑色素瘤的发展，至少从其最常见的一个等位基因缺失和/或另一个等位基因突变的机制来看是这样。 (C) 1993 Wiley-Liss, Inc.
To investigate the role of the p53 tumor-suppressor gene in the development of human melanoma, loss of heterozygosity (LOH) of p53 was studied in 46 cases of melanoma by a polymerase-chain-reaction/restriction-fragment-length polymorphism (PCR/RFLP) analysis, and p53 mutations were assessed in 51 cases of melanoma by a polymerase-chain-reaction/ single-strand-conformation polymorphism (PCR/SSCP) analysis. Frozen tumors and paraffin samples were used in the study. We were not able to detect any allelic loss in 12 BstUI informative cases or any single mutation in exons 5 to 8 of the p53 gene. Our results, together with other findings at the DNA level, suggest that the p53 gene appears not to be commonly involved in the development of melanoma, at least by its most frequent mechanisms of deletion of one allele and/or mutation in the other. (C) 1993 Wiley-Liss, Inc.