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作 者:姚书娜(综述)[1] 刘艳艳(审校)[1] 杨树军(审校)[1]
出 处:《国际肿瘤学杂志》2009年第10期763-765,共3页Journal of International Oncology
摘 要:PTEN在肿瘤中存在基因组、基因转录、翻译和翻译后等多个水平的异常,从而导致P13K/Akt通路的过度激活。这不仅是肿瘤发生的重要机制,也与某些靶向治疗后的耐药相关。克服PTEN异常所致耐药的方法包括直接应用作用于P13K/Akt通路的新型靶向药物以及重新恢复PTEN基因的表达和功能。PTEN is a powerful tumor suppressor gene located at chromosome 10q23, which exists multi-level abnormalities in cancer, including genome, gene transcription, protein translation and post-translation, which can result in overactivation of PI3K/Akt pathway. They are not only related to tumorigenesis, but also associated with resistance to targeted drugs in cancer. When it comes to overcome the resistance, novel PI3K/ Akt pathway inhibitors and approaches to restore the expression and function of PTEN may be considered.
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