Frequency of Smad gene mutations in human cancers.
Frequency of Smad gene mutations in human cancers.
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DOI：
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发表时间：
1997-07
期刊：
影响因子：
11.2
通讯作者：
G. Riggins;K. Kinzler;B. Vogelstein;S. Thiagalingam
中科院分区：
文献类型：
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作者：
G. Riggins;K. Kinzler;B. Vogelstein;S. Thiagalingam
Smad基因的发现最近引起了很大的兴奋，Smad基因编码的蛋白质抑制来自细胞因子转化生长因子β家族的信号。在这里，我们报告完成克隆的六个已知的人类Smads，提供新的序列Smad5和Smad6。以前，Smad4和Smad2在人类癌症中被证明是突变的。然而，对其他四个Smad基因的分析显示，在总共167个肿瘤中没有突变，包括来自结肠、乳腺、肺和胰腺的肿瘤。这些结果表明，不同的Smad基因具有不同的功能，并表明这四个基因的突变一般不解释在人类肿瘤中发现的对转化生长因子β的广泛抗性。
Much excitement has recently been generated by the discovery of the Smad genes, encoding proteins that transduce signals from the transforming growth factor beta family of cytokines. Here, we report the completion of cloning of the six known human Smads, providing novel sequences for Smad5 and Smad6. Previously, Smad4 and Smad2 were shown to be mutated in human cancers. However, analysis of the other four Smad genes revealed no mutations in a total of 167 tumors, including those from colon, breast, lung, and pancreas. These results suggest that the various Smad genes have different functions and demonstrate that mutations in these four genes do not, in general, account for the widespread resistance to transforming growth factor beta that is found in human tumors.