Suppr超能文献

PI3K/AKT/mTOR通路的激活导致乳腺癌耐药。

Activation of PI3K/AKT/mTOR Pathway Causes Drug Resistance in Breast Cancer.

作者信息

Dong Chao, Wu Jiao, Chen Yin, Nie Jianyun, Chen Ceshi

机构信息

Department of the Second Medical Oncology, The 3rd Affiliated Hospital of Kunming Medical University, Yunnan Tumor Hospital, Kunming, China.

Department of Urology, Changhai Hospital, Navy Medical University, Shanghai, China.

出版信息

Front Pharmacol. 2021 Mar 15;12:628690. doi: 10.3389/fphar.2021.628690. eCollection 2021.

Abstract

Although chemotherapy, targeted therapy and endocrine therapy decrease rate of disease recurrence in most breast cancer patients, many patients exhibit acquired resistance. Hyperactivation of the PI3K/AKT/mTOR pathway is associated with drug resistance and cancer progression. Currently, a number of drugs targeting PI3K/AKT/mTOR are being investigated in clinical trials by combining them with standard therapies to overcome acquired resistance in breast cancer. In this review, we summarize the critical role of the PI3K/AKT/mTOR pathway in drug resistance, the development of PI3K/AKT/mTOR inhibitors, and strategies to overcome acquired resistance to standard therapies in breast cancer.

摘要

尽管化疗、靶向治疗和内分泌治疗可降低大多数乳腺癌患者的疾病复发率,但许多患者会出现获得性耐药。PI3K/AKT/mTOR通路的过度激活与耐药性及癌症进展相关。目前,一些靶向PI3K/AKT/mTOR的药物正在临床试验中进行研究,将它们与标准疗法联合使用以克服乳腺癌的获得性耐药。在本综述中,我们总结了PI3K/AKT/mTOR通路在耐药性中的关键作用、PI3K/AKT/mTOR抑制剂的研发情况,以及克服乳腺癌对标准疗法获得性耐药的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5430/8005514/fddb94152d60/fphar-12-628690-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验