ArticleCancer letters2019
Estrogen-independent Myc overexpression confers endocrine therapy resistance on breast cancer cells expressing ERαY537S and ERαD538G mutations.
Article in Cancer letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- FGD3 mediates lytic cell death, enhancing efficacy and immunogenicity of chemotherapy agents in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- A necrosis inducer promotes an immunogenic response and destroys ovarian cancers in mouse xenografts and patient ascites organoids.Cancer letters · 2025Article
- GNA13 suppresses proliferation of ER+ breast cancer cells via ERα dependent upregulation of the MYC oncogene.Breast cancer research : BCR · 2024Article
- Spatiotemporal Control of Inflammatory Lytic Cell Death Through Optogenetic Induction of RIPK3 Oligomerization.Journal of molecular biology · 2024Article
- The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer.Cell death and differentiation · 2024Article
- Plasma Membrane Channel TRPM4 Mediates Immunogenic Therapy-Induced Necrosis.Cancer research · 2023Article
- An Autophagy-Associated Prognostic Gene Signature for Breast Cancer.Biochemical genetics · 2023Article
- Cell facilitation promotes growth and survival under drug pressure in breast cancer.Nature communications · 2023Article
- FOXA1 Reprogramming Dictates Retinoid X Receptor Response in ESR1-Mutant Breast Cancer.Molecular cancer research : MCR · 2023Article
- Non-Coding RNAs Modulating Estrogen Signaling and Response to Endocrine Therapy in Breast Cancer.Cancers · 2023Review
- Article
- ESR1 mutant breast cancers show elevated basal cytokeratins and immune activation.Nature communications · 2022Article
- Hotspot ESR1 Mutations Are Multimodal and Contextual Modulators of Breast Cancer Metastasis.Cancer research · 2022Article
- Epigenetic Mechanisms Influencing Therapeutic Response in Breast Cancer.Frontiers in oncology · 2022Review
- ESR1 fusions and therapeutic resistance in metastatic breast cancer.Frontiers in oncology · 2022Review
- Inhibition of Metabolism as a Therapeutic Option for Tamoxifen-Resistant Breast Cancer Cells.Cells · 2021Article
- A small-molecule activator of the unfolded protein response eradicates human breast tumors in mice.Science translational medicine · 2021Article
- Steroid Hormone Receptor and Infiltrating Immune Cell Status Reveals Therapeutic Vulnerabilities ofCancer research · 2021Article
- Estrogen Receptor Alpha Mutations in Breast Cancer Cells Cause Gene Expression Changes through Constant Activity and Secondary Effects.Cancer research · 2021Article
- Identification of a Transcription Factor Signature That Can Predict Breast Cancer Survival.Computational and mathematical methods in medicine · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Approximately 30% of metastatic breast cancers harbor estrogen receptor α (ERα) mutations associated with resistance to endocrine therapy and reduced survival. Consistent with their constitutive proliferation, T47D and MCF7 cells in which wild-type ERα is replaced by the most common mutations, ERαY537S and ERαD538G, exhibit partially estrogen-independent gene expression. A novel invasion/dissociation/rebinding assay demonstrated that the mutant cells have a higher tendency to dissociate from invasion sites and rebind to a second site. Compared to ERαD538G breast tumors, ERαY537S tumors exhibited a dramatic increase in lung metastasis. Transcriptome analysis showed that the ERαY537S and ERαD538G mutations each elicit a unique gene expression profile. Gene set enrichment analysis showed Myc target pathways are highly induced in mutant cells. Moreover, chromatin immunoprecipitation showed constitutive, fulvestrant-resistant, recruitment of ERα mutants to the Myc enhancer region, resulting in estrogen-independent Myc overexpression in mutant cells and tumors. Knockdown and virus transduction showed Myc is necessary and sufficient for ligand-independent proliferation of the mutant cells but had no effect on metastasis-related phenotypes. Thus, Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations.
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