Advances in Brief p 53 Mutation and MDM 2 Amplification in Human Soft Tissue Sarcomas 1
Advances in Brief p 53 Mutation and MDM 2 Amplification in Human Soft Tissue Sarcomas 1
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发表时间：
2006
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通讯作者：
F. Leach;T. Tokino;P. 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;P. Meltzer;M. Burrell;J. Oliner;Sharon Smith;D. Hill;D. Sidransky;K. Kinzler;B. Vogelstein
对24例软组织肉瘤(11例恶性纤维组织细胞瘤和13例脂肪肉瘤)进行了P53和MDM2基因检测。在1/3(8/24)的肉瘤中检测到P53的异常，包括点突变、缺失或过度表达。另有8例肿瘤组织中检测到MDM2基因扩增，但未发现两种基因同时发生改变。制备了与人MDM2基因产物反应的单抗，免疫组织化学分析显示MI1M2在扩增MDM2基因的肿瘤中有核定位和MI1M2过表达。这些数据支持P53和MDM2基因改变是抑制细胞生长的同一调控途径失活的替代机制的假设。
The p53 and MDM2 genes were analyzed in 24 human soft tissue sarcomas (11 malignant fibrous histiocytomas and 13 liposarcomas). Al terations 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 hu man MDM2 gene product were developed, and ¡mmunohistochemical analysis revealed nuclear localization and overexpression of MI1M2 in those tumors with amplified MDM2 genes. These data support the hy pothesis that p53 and MDM2 genetic alterations are alternative mecha nisms for inactivating the same regulatory pathway for suppressing cell growth.