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Review
. 2020 Nov 10;12(11):3323.
doi: 10.3390/cancers12113323.

Mechanisms of Taxane Resistance

Affiliations
Review

Mechanisms of Taxane Resistance (VSports)

Sara M Maloney (VSports注册入口) et al. Cancers (Basel). .

Abstract (VSports在线直播)

The taxane family of chemotherapy drugs has been used to treat a variety of mostly epithelial-derived tumors and remain the first-line treatment for some cancers VSports手机版. Despite the improved survival time and reduction of tumor size observed in some patients, many have no response to the drugs or develop resistance over time. Taxane resistance is multi-faceted and involves multiple pathways in proliferation, apoptosis, metabolism, and the transport of foreign substances. In this review, we dive deeper into hypothesized resistance mechanisms from research during the last decade, with a focus on the cancer types that use taxanes as first-line treatment but frequently develop resistance to them. Furthermore, we will discuss current clinical inhibitors and those yet to be approved that target key pathways or proteins and aim to reverse resistance in combination with taxanes or individually. Lastly, we will highlight taxane response biomarkers, specific genes with monitored expression and correlated with response to taxanes, mentioning those currently being used and those that should be adopted. The future directions of taxanes involve more personalized approaches to treatment by tailoring drug-inhibitor combinations or alternatives depending on levels of resistance biomarkers. We hope that this review will identify gaps in knowledge surrounding taxane resistance that future research or clinical trials can overcome. .

Keywords: breast cancer; ovarian cancer; prostate cancer; taxane resistance. V体育安卓版.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Overview of taxane resistance mechanisms. This diagram illustrates some of the major proteins and pathways that are known to contribute to taxane resistance in cancer. Upregulated pro-survival pathways, induction of EMT through upregulated vimentin, ZEB1, and TGF-β, and upregulated anti-apoptotic proteins have been linked with increased proliferation after taxane treatment. Upregulated tubulin isotypes, drug export transporters, and drug-metabolizing enzymes have been associated with reduced taxane efficacy. Hypoxia and non-coding RNAs have been noted to activate some of the established resistance mechanisms, so they will be considered to be contributing factors to taxane resistance as well. The review will include these mechanisms and others, which are frequently observed in different cancer types. Figure was made in BioRender.

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