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乳腺癌中的磷脂酰肌醇 3-激酶/AKT 信号通路。

The phosphatidyl inositol 3-kinase/AKT signaling pathway in breast cancer.

机构信息

Instituto Nacional Enfermedades Neoplásicas, Lima, Peru.

出版信息

Cancer Metastasis Rev. 2010 Dec;29(4):751-9. doi: 10.1007/s10555-010-9261-0.

Abstract

The phosphatidyl inositol 3-kinase (PI3K)/Akt pathway mediates the effects of a variety of extracellular signals in a number of cellular processes including cell growth, proliferation, and survival. The alteration of integrants of this pathway through mutation of its coding genes increases the activation status of the signaling and can thus lead to cellular transformation. The frequent dysregulation of the PI3K/Akt pathway in breast cancer (BC) and the mediation of this pathway in different processes characteristically implicated in tumorigenesis have attracted the interest of this pathway in BC; however, a more comprehensive understanding of the signaling intricacies is necessary to develop clinical applications of the modulation of this pathway in this pathology. We review a series of experiments examining the contribution of alteration of integrants of this signaling network to human BC and we make an update of the information about the effect of the modulation of this pathway in this cancer.

摘要

磷脂酰肌醇 3-激酶 (PI3K)/Akt 途径介导多种细胞过程中各种细胞外信号的作用,包括细胞生长、增殖和存活。该途径的整合子通过其编码基因的突变而改变,会增加信号的激活状态,从而导致细胞转化。PI3K/Akt 途径在乳腺癌 (BC) 中的频繁失调,以及该途径在肿瘤发生过程中不同特征中的介导作用,引起了人们对该途径在 BC 中的关注;然而,为了在该病理学中开发该途径调节的临床应用,需要更全面地了解信号的复杂性。我们回顾了一系列检查改变该信号网络整合子对人类 BC 的贡献的实验,并更新了关于该途径在这种癌症中的调节作用的信息。

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