ArticleCancer drug resistance (Alhambra, Calif.)2021
Experimental models of endocrine responsive breast cancer: strengths, limitations, and use.
Article in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Sensitive detection of unopposed estrogen using estrogen receptor functionalized nanoprobes for cancer diagnosis.Discover nano · 2026Review
- Synergistic Potential of Organotin(IV) Carbodithioate Derivatives with Vitamins D and E in MCF-7 and MDA-MB-231 Breast Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Oestrogen changes at menopause: insights into obesity-associated breast risk and outcomes.Nature reviews. Endocrinology · 2026Review
- Exploring the Cytotoxic and Redox-Modulatory Effects of Nanoceria in MCF7 Breast Cancer Cells Using Integrated Molecular and Proteomic Analyses.Antioxidants (Basel, Switzerland) · 2025Article
- Synergistic targeting of cancer-related proteins by benzyl isothiocyanate and caffeic acid: MLSD and cytotoxic mechanisms in MCF-7 cells.3 Biotech · 2025Article
- Review
- Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024Review
- S-Allyl-L-Cysteine Affects Cell Proliferation and Expression of HBiomolecules · 2024Article
- Autophagy and senescence facilitate the development of antiestrogen resistance in ER positive breast cancer.Frontiers in endocrinology · 2024Review
- Upregulation of the EGFR/MEK1/MAPK1/2 signaling axis as a mechanism of resistance to antiestrogen‑induced BimEL dependent apoptosis in ERInternational journal of oncology · 2023Article
- Introduction: Cancer Systems and Integrative Biology.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Targeting hormone-resistant breast cancer cells with docetaxel: a look inside the resistance.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Characterization of HCI-EC-23 a novel estrogen- and progesterone-responsive endometrial cancer cell line.Scientific reports · 2022Article
- Inhibitor of glutamine metabolism V9302 promotes ROS-induced autophagic degradation of B7H3 to enhance antitumor immunity.The Journal of biological chemistry · 2022Article
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Breast cancers characterized by expression of estrogen receptor-alpha; ESR1) represent approximately 70% of all new cases and comprise the largest molecular subtype of this disease. Despite this high prevalence, the number of adequate experimental models of ER+ breast cancer is relatively limited. Nonetheless, these models have proved very useful in advancing understanding of how cells respond to and resist endocrine therapies, and how the ER acts as a transcription factor to regulate cell fate signaling. We discuss the primary experimental models of ER+ breast cancer including 2D and 3D cultures of established cell lines, cell line- and patient-derived xenografts, and chemically induced rodent models, with a consideration of their respective general strengths and limitations. What can and cannot be learned easily from these models is also discussed, and some observations on how these models may be used more effectively are provided. Overall, despite their limitations, the panel of models currently available has enabled major advances in the field, and these models remain central to the ability to study mechanisms of therapy action and resistance and for hypothesis testing that would otherwise be intractable or unethical in human subjects.
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Registered trials
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.