ArticleThe Journal of steroid biochemistry and molecular biology
Mechanisms of acquired resistance to endocrine therapy in hormone-dependent breast cancer cells.
Article in The Journal of steroid biochemistry and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 116 citations in OpenAlex.
- Effect of everolimus on bone marker levels and progressive disease in bone in BOLERO-2.Journal of the National Cancer Institute · 2013Trial
- A phase II trial of capecitabine in combination with the farnesyltransferase inhibitor tipifarnib in patients with anthracycline-treated and taxane-resistant metastatic breast cancer: an Eastern Cooperative Oncology Group Study (E1103).Breast cancer research and treatment · 2012Trial
- Phase II trial of the farnesyltransferase inhibitor tipifarnib plus fulvestrant in hormone receptor-positive metastatic breast cancer: New York Cancer Consortium Trial P6205.Annals of oncology : official journal of the European Society for Medical Oncology · 2009Trial
- Multimodal diagnostic models and subtype analysis for neoadjuvant therapy in breast cancer.Frontiers in immunology · 2025Article
- Targeting Breast Cancer: The Familiar, the Emerging, and the Uncharted Territories.Biomolecules · 2023Review
- Adrenal Steroids and Resistance to Hormonal Blockade of Prostate and Breast Cancer.Endocrinology · 2023Review
- miR-489 Confines Uncontrolled Estrogen Signaling through a Negative Feedback Mechanism and Regulates Tamoxifen Resistance in Breast Cancer.International journal of molecular sciences · 2022Article
- Article
- Review
- Exploring Biomarkers of Phosphoinositide 3-Kinase Pathway Activation in the Treatment of Hormone Receptor Positive, Human Epidermal Growth Receptor 2 Negative Advanced Breast Cancer.The oncologist · 2019Review
- Isobavachalcone sensitizes cells to E2-induced paclitaxel resistance by down-regulating CD44 expression in ER+ breast cancer cells.Journal of cellular and molecular medicine · 2018Article
- Re-adopting classical nuclear receptors by cholesterol metabolites.The Journal of steroid biochemistry and molecular biology · 2016Review
- The best of both worlds - managing the cancer, saving the bone.Nature reviews. Endocrinology · 2016Review
- Efficacy of SERD/SERM Hybrid-CDK4/6 Inhibitor Combinations in Models of Endocrine Therapy-Resistant Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- VAV3 mediates resistance to breast cancer endocrine therapy.Breast cancer research : BCR · 2014Article
- GPR30 as an initiator of tamoxifen resistance in hormone-dependent breast cancer.Breast cancer research : BCR · 2013Article
- Clinical instability of breast cancer markers is reflected in long-term in vitro estrogen deprivation studies.BMC cancer · 2013Article
- Everolimus in postmenopausal, hormone receptor-positive advanced breast cancer: summary and results of an austrian expert panel discussion.Breast care (Basel, Switzerland) · 2013Review
- The phosphoinositide-3-kinase-Akt-mTOR pathway as a therapeutic target in breast cancer.Journal of the National Comprehensive Cancer Network : JNCCN · 2013Review
- The role of mammalian target of rapamycin (mTOR) inhibition in the treatment of advanced breast cancer.Current oncology reports · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Acquired resistance is a major problem limiting the clinical benefit of endocrine therapy. To investigate the mechanisms involved, two in vitro models were developed from MCF-7 cells. Long-term culture of MCF-7 cells in estrogen deprived medium (LTED) mimics aromatase inhibition in patients. Continued exposure of MCF-7 to tamoxifen represents a model of acquired resistance to antiestrogens (TAM-R). Long-term estrogen deprivation results in sustained activation of the ERK MAP kinase and the PI3 kinase/mTOR pathways. Using a novel Ras inhibitor, farnesylthiosalicylic acid (FTS), to achieve dual inhibition of the pathways, we found that the mTOR pathway plays the primary role in mediation of proliferation of LTED cells. In contrast to the LTED model, there is no sustained activation of ERK MAPK but enhanced responsiveness to rapid stimulation induced by E(2) and TAM in TAM-R cells. An increased amount of ERalpha formed complexes with EGFR and c-Src in TAM-R cells, which apparently resulted from extra-nuclear redistribution of ERalpha. Blockade of c-Src activity drove ERalpha back to the nucleus and reduced ERalpha-EGFR interaction. Prolonged blockade of c-Src activity restored sensitivity of TAM-R cells to tamoxifen. Our results suggest that different mechanisms are involved in acquired endocrine resistance and the necessity for individualized treatment of recurrent diseases.
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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.