ArticleBMC cancer2016
Systematic drug screening reveals specific vulnerabilities and co-resistance patterns in endocrine-resistant breast cancer.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Cannabidiol enhances tamoxifen efficacy via CREB-mediated suppression of ERα signaling in ER-positive breast cancer cells.Cell & bioscience · 2026Article
- Distinct molecular profiles and shared drug vulnerabilities in pancreatic metastases of renal cell carcinoma.Communications biology · 2024Article
- Monopolar spindle 1 contributes to tamoxifen resistance in breast cancer through phosphorylation of estrogen receptor α.Breast cancer research and treatment · 2023Article
- Compressive stress-mediated p38 activation required for ERα + phenotype in breast cancer.Nature communications · 2021Article
- Review
- Experimental models of endocrine responsive breast cancer: strengths, limitations, and use.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Although c‑MYC contributes to tamoxifen resistance, it improves cisplatin sensitivity in ER‑positive breast cancer.International journal of oncology · 2020Article
- High content phenotypic screening identifies serotonin receptor modulators with selective activity upon breast cancer cell cycle and cytokine signaling pathways.Bioorganic & medicinal chemistry · 2020Article
- A multitargeted probe-based strategy to identify signaling vulnerabilities in cancers.The Journal of biological chemistry · 2019Article
- Inhibition of histone methyltransferase DOT1L silences ERα gene and blocks proliferation of antiestrogen-resistant breast cancer cells.Science advances · 2019Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe estrogen receptor (ER) inhibitor tamoxifen reduces breast cancer mortality by 31 % and has served as the standard treatment for ER-positive breast cancers for decades. However, 50 % of advanced ER-positive cancers display de novo resistance to tamoxifen, and acquired resistance evolves in 40 % of patients who initially respond. Mechanisms underlying resistance development remain poorly understood and new therapeutic opportunities are urgently needed. Here, we report the generation and characterization of seven tamoxifen-resistant breast cancer cell lines from four parental strains.
methodsUsing high throughput drug sensitivity and resistance testing (DSRT) with 279 approved and investigational oncology drugs, exome-sequencing and network analysis, we for the first time, systematically determine the drug response profiles specific to tamoxifen resistance.
resultsWe discovered emerging vulnerabilities towards specific drugs, such as ERK1/2-, proteasome- and BCL-family inhibitors as the cells became tamoxifen-resistant. Co-resistance to other drugs such as the survivin inhibitor YM155 and the chemotherapeutic agent paclitaxel also occurred.
conclusionThis study indicates that multiple molecular mechanisms dictate endocrine resistance, resulting in unexpected vulnerabilities to initially ineffective drugs, as well as in emerging co-resistances. Thus, combatting drug-resistant tumors will require patient-tailored strategies in order to identify new drug vulnerabilities, and to understand the associated co-resistance patterns.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.