Targeting of estrogen receptor is commonly used as a first-line treatment for hormone-positive breast cancer patients, and is considered as a keystone of systemic cancer therapy. Likewise, HER2-targeted therapy significantly improved the survival of HER2-positive breast cancer patients, indicating that targeted therapy is a powerful therapeutic strategy for breast cancer. However, for triple-negative breast cancer (TNBC), an aggressive breast cancer subtype, there are no clinically approved targeted therapies, and thus, an urgent need to identify potent, highly effective therapeutic targets. In this mini-review, we describe general strategies to inhibit tumor growth by targeted therapies and briefly discuss emerging resistance mechanisms. Particularly, we focus on therapeutic targets for TNBC and discuss combination therapies targeting the epidermal growth factor receptor (EGFR) and associated resistance mechanisms.
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Cover Image
Cover Image
The cover shows a metaphorical representation of the anti-CRISPR AcrIIA6, represented as handcuffs, sequestering two Streptococcus thermophilus CRISPR1-Cas9 (St1Cas9) molecules at a time and preventing conformational changes associated with DNA recognition and binding. In the absence of AcrIIA6, St1Cas9 tightly binds to its target DNA, and can proceed to target cleavage. For further information, see the article by Hardouin and Goulet in this issue (pp. 507–516). This cover artwork has been made by Beata Edyta Mierzwa (www.BeataScienceArt.com).
Targeted therapy and drug resistance in triple-negative breast cancer: the EGFR axis
Sima Lev; Targeted therapy and drug resistance in triple-negative breast cancer: the EGFR axis. Biochem Soc Trans 29 April 2020; 48 (2): 657–665. doi: https://doi.org/10.1042/BST20191055
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