Molecular mechanisms of drug resistance of glial tumor of brain. Part 2: Proliferation, angiogenesis, metastasis and recurrency

A. Chernov, E. Galimova, O. Shamova
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Abstract

The main reason for the low efficiency of glioblastoma therapy is its resistance to therapeutic procedures. The development of multidrug resistance occurs as a result of the selection of tumor clones during therapy. The resistant cell clones to radiotherapy and chemotherapy can proliferate, leading to tumor growth, in which its own vascular network is formed (angiogenesis), which promotes cell migration, invasion and the appearance of metastases and recurrent glioblastoma. The review examines the relationship at the molecular level of multidrug resistance with proliferation, angiogenesis, migration, metastasis, and the formation of glioblastoma relapses, with an emphasis on identifying new targets among proteins, microRNAs, signal transduction kinases, transcription factors, tumor-supressor genes and oncogenes.
脑胶质肿瘤耐药的分子机制。第二部分:增殖、血管生成、转移和复发
胶质母细胞瘤治疗效率低的主要原因是其对治疗程序的抗性。多药耐药的发生是治疗过程中肿瘤克隆选择的结果。放疗和化疗的耐药细胞克隆可以增殖,导致肿瘤生长,在肿瘤生长过程中形成自身的血管网络(血管生成),促进细胞迁移、侵袭,出现转移和复发的胶质母细胞瘤。本文综述了多药耐药在分子水平上与胶质母细胞瘤增殖、血管生成、迁移、转移和复发形成的关系,重点在蛋白质、microrna、信号转导激酶、转录因子、肿瘤抑制基因和癌基因中发现新的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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