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首页> 外文期刊>Expert opinion on therapeutic targets >Akt as a therapeutic target in cancer.
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Akt as a therapeutic target in cancer.

机译：Akt作为癌症的治疗靶标。

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BACKGROUND: The phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) pathway is central in the transmission of growth regulatory signals originating from cell surface receptors. OBJECTIVE: This review discusses how mutations occur that result in elevated expression the PI3K/PTEN/Akt/mTOR pathway and lead to malignant transformation, and how effective targeting of this pathway may result in suppression of abnormal growth of cancer cells. METHODS: We searched the literature for articles which dealt with altered expression of this pathway in various cancers including: hematopoietic, melanoma, non-small cell lung, pancreatic, endometrial and ovarian, breast, prostate and hepatocellular. RESULTS/CONCLUSIONS: The PI3K/PTEN/Akt/mTOR pathway is frequently aberrantly regulated in various cancers and targeting this pathway with small molecule inhibitors and may result in novel, more effective anticancer therapies.
机译：背景：磷脂酰肌醇3-激酶（PI3K）/磷酸酶和张力蛋白同源物（PTEN）/ v-akt鼠胸腺瘤病毒致癌基因同源物（Akt）/雷帕霉素哺乳动物靶标（mTOR）途径在源于生长调节信号的传递中起着中心作用细胞表面受体。目的：本综述讨论突变如何发生，从而导致PI3K / PTEN / Akt / mTOR途径表达升高并导致恶性转化，以及有效靶向该途径如何抑制癌细胞的异常生长。方法：我们在文献中搜索了有关该途径在多种癌症中表达改变的文章，包括：造血，黑色素瘤，非小细胞肺癌，胰腺癌，子宫内膜和卵巢癌，乳腺癌，前列腺癌和肝细胞癌。结果/结论：PI3K / PTEN / Akt / mTOR途径在各种癌症中经常受到异常调节，并以小分子抑制剂靶向该途径，并可能导致新型，更有效的抗癌治疗。

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