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首页> 外文期刊>Journal of Cellular Physiology >MET receptor is overexpressed but not mutated in oral squamous cell carcinomas.
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MET receptor is overexpressed but not mutated in oral squamous cell carcinomas.

机译:满足受体中而不是突变口腔鳞状细胞癌。

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摘要

Oral squamous cell carcinoma (SCC) is a neoplasm characterized by a high degree of local invasion and an elevated rate of metastasis to cervical lymph nodes. It has been shown that the Hepatocyte Growth Factor/Scatter Factor Receptor Met is constitutively activated in many human tumors of epithelial origin and that it plays a critical role to confer invasive properties to neoplastic cells. Most frequently, Met activation is due to receptor overexpression, but also point mutations in the tyrosine kinase domain can lead to deregulated activation. Here we show that in all the primary tumors examined this receptor is overexpressed. Direct sequencing of Met mRNAs failed to find any activating mutation in its intracellular domain. Moreover, in cell lines derived from squamous cell carcinomas, HGF-induced activation of Met resulted in the acquisition of invasive properties. All together these data suggest that the MET oncogene is involved in progression of squamous cell carcinoma toward an invasive-metastatic behavior. Copyright 2001 Wiley-Liss, Inc.
机译:口腔鳞状细胞癌(SCC)是一个肿瘤特点是高度的当地的入侵和一个颈转移率的提升淋巴结。肝细胞生长因子/散射因子受体遇到了许多人类持续激活上皮来源的肿瘤,它扮演了一个关键角色授予入侵属性肿瘤细胞。是由于受体过度,但也点吗酪氨酸激酶域会导致突变放松管制的激活。所有的主要肿瘤检查这种受体过表达。没有找到任何激活突变的胞内域。来源于鳞状细胞癌,HGF-induced激活导致会面收购侵入性属性。这些数据表明,大都会致癌基因参与的鳞状细胞癌向invasive-metastatic行为。版权2001 Wiley-Liss公司。

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