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modifications to the structure of the egf receptor gene in human glioma

机译:胶质瘤中egf受体基因结构的修饰

摘要

The epidermal growth factor receptor (EGFR) gene is amplified in 40% of malignant gliomas and the amplified genes are frequently rearranged. The genetic alterations associated with these rearrangements are characterized in five malignant gliomas. In one tumor, the rearrangement resulted in the deletion of most of the extracytoplasmic domain of the receptor, resulting in a hybrid mRNA between new sequences and the truncated EGFR. The predicted amino acid sequence of the protein from this tumor was remarkably similar to that described for several viral erb-B oncogenes. Four other tumors were noted to have internal deletions of the EGF receptor gene. These rearrangements brought about in-frame deletions affecting either of two cysteine-rich domains in the extracytoplasmic portion of the molecule. The clonal nature of these alterations, and the fact that identical alterations were seen in more than one tumor, suggests a role for these mutant receptor proteins in tumorigenesis. Furthermore, these studies document the existence of tumor specific cell molecules resulting from somatic mutation.
机译:表皮生长因子受体(EGFR)基因在40%的恶性神经胶质瘤中扩增,并且扩增后的基因经常重新排列。与这些重排相关的遗传改变的特征在于五种恶性神经胶质瘤。在一种肿瘤中,重排导致受体大部分胞质外结构域的缺失,从而导致新序列与截短的EGFR之间存在杂交mRNA。该肿瘤蛋白质的预测氨基酸序列与几种病毒erb-B癌基因的描述非常相似。注意到另外四个肿瘤具有EGF受体基因的内部缺失。这些重排导致框内缺失,其影响分子胞质外部分中两个富含半胱氨酸的结构域中的一个。这些改变的克隆性质,以及在一个以上的肿瘤中观察到相同的改变,这一事实表明了这些突变受体蛋白在肿瘤发生中的作用。此外,这些研究记录了由体细胞突变导致的肿瘤特异性细胞分子的存在。

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