ArticleBreast cancer research : BCR2018
Targeting tumour re-wiring by triple blockade of mTORC1, epidermal growth factor, and oestrogen receptor signalling pathways in endocrine-resistant breast cancer.
Article in Breast cancer research : BCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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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.
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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.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Efficacy and Determinants of Response to HER Kinase Inhibition inCancer discovery · 2020Trial
- ROS-Fueled Allies: STAT3, PKM2, and HIF-1α Influencing Energy Metabolism in Hormone-Independent Cancers.International journal of molecular sciences · 2026Article
- Comparative efficacy of Palbociclib and Everolimus with aromatase inhibitors in second line treatment of HR and HER2 negative metastatic breast cancer.Discover oncology · 2025Article
- Correction: Targeting tumour re-wiring by triple blockade of mTORC1, epidermal growth factor, and oestrogen receptor signalling pathways in endocrine-resistant breast cancer.Breast cancer research : BCR · 2025Article
- Characteristic Binding Landscape of Estrogen Receptor-α36 Protein Enhances Promising Cancer Drug Design.Biomolecules · 2023Article
- Molecular profiling of aromatase inhibitor sensitive and resistant ER+HER2- postmenopausal breast cancers.Nature communications · 2023Article
- Estrogen/HER2 receptor crosstalk in breast cancer: combination therapies to improve outcomes for patients with hormone receptor-positive/HER2-positive breast cancer.NPJ breast cancer · 2023Review
- Targeting miRNAs and Other Non-Coding RNAs as a Therapeutic Approach: An Update.Non-coding RNA · 2023Review
- Association of functional genetic variants in TFF1 and nephrolithiasis risk in a Chinese population.BMC urology · 2022Article
- Article
- Regulation of aromatase in cancer.Molecular and cellular biochemistry · 2021Review
- MicroRNAs and Long Noncoding RNAs as Novel Therapeutic Targets in Estrogen Receptor-Positive Breast and Ovarian Cancers.International journal of molecular sciences · 2021Review
- RON signalling promotes therapeutic resistance in ESR1 mutant breast cancer.British journal of cancer · 2021Article
- Review
- Advances in the Detection Technologies and Clinical Applications of Circulating Tumor DNA in Metastatic Breast Cancer.Cancer management and research · 2020Review
- Combination of mTORC1/2 inhibitor vistusertib plus fulvestrant in vitro and in vivo targets oestrogen receptor-positive endocrine-resistant breast cancer.Breast cancer research : BCR · 2019Article
- Chlorotoxin targets ERα/VASP signaling pathway to combat breast cancer.Cancer medicine · 2019Article
- Clinical and genetic risk factors for Fulvestrant treatment in post-menopause ER-positive advanced breast cancer patients.Journal of translational medicine · 2019Article
- Endocrine Resistance in Hormone Receptor Positive Breast Cancer-From Mechanism to Therapy.Frontiers in endocrinology · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndocrine therapies are the mainstay of treatment for oestrogen receptor (ER)-positive (ER
methodsA panel of ER
resultsHere, we show RAD001 and neratinib (pan-ERBB inhibitor) caused a concentration-dependent decrease in proliferation, irrespective of the ESR1 mutation status. The combination of either agent with endocrine therapy further reduced proliferation but the maximum effect was observed with a triple combination of RAD001, neratinib, and endocrine therapy. In the absence of oestrogen, RAD001 caused a reduction in ER-mediated transcription in the majority of the cell lines, which associated with a decrease in recruitment of ER to an oestrogen-response element on the TFF1 promoter. Contrastingly, neratinib increased both ER-mediated transactivation and ER recruitment, an effect reduced by the addition of RAD001. In-vivo analysis of an LTED model showed the triple combination of RAD001, neratinib, and fulvestrant was most effective at reducing tumour volume. Gene set enrichment analysis revealed that the addition of neratinib negated the epidermal growth factor (EGF)/EGF receptor feedback loops associated with RAD001.
conclusionsOur data support the combination of therapies targeting ERBB2/3 and mTORC1 signalling, together with fulvestrant, in patients who relapse on endocrine therapy and retain a functional ER.
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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.