p53 Mutation and MDM2 amplification in human soft tissue sarcomas.
p53 Mutation and MDM2 amplification in human soft tissue sarcomas.
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发表时间：
1993-05
期刊：
影响因子：
11.2
通讯作者：
F. Leach;T. Tokino;T. Tokino;Paul A. Meltzer;M. Burrell;J. Oliner;Sharon Smith;D. Hill;D. Sidransky;K. Kinzler;B. Vogelstein
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作者：
F. Leach;T. Tokino;T. Tokino;Paul A. Meltzer;M. Burrell;J. Oliner;Sharon Smith;D. Hill;D. Sidransky;K. Kinzler;B. Vogelstein
对24例软组织肉瘤（恶性纤维组织细胞瘤11例，脂肪肉瘤13例）进行p53和MDM2基因检测。在三分之一（24例中的8例）的肉瘤中检测到p53的改变，包括点突变、缺失或过表达。在另外8例肿瘤中检测到MDM2基因扩增，但没有肿瘤包含两个基因的改变。与人MDM2基因产物反应的单克隆抗体被开发出来，免疫组织化学分析显示，在MDM2基因扩增的肿瘤中，MDM2的核定位和过表达。这些数据支持这一假设，即p53和MDM2基因改变是灭活抑制细胞生长的相同调节途径的替代机制。
The p53 and MDM2 genes were analyzed in 24 human soft tissue sarcomas (11 malignant fibrous histiocytomas and 13 liposarcomas). Alterations of p53, consisting of point mutations, deletions, or overexpression, were detected in one-third (8 of 24) of the sarcomas. MDM2 gene amplification was detected in another 8 tumors, but no tumor contained an alteration of both genes. Monoclonal antibodies reactive with the human MDM2 gene product were developed, and immunohistochemical analysis revealed nuclear localization and overexpression of MDM2 in those tumors with amplified MDM2 genes. These data support the hypothesis that p53 and MDM2 genetic alterations are alternative mechanisms for inactivating the same regulatory pathway for suppressing cell growth.