ArticleFEBS letters2013
Modeling the estrogen receptor to growth factor receptor signaling switch in human breast cancer cells.
Article in FEBS letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- The Pivotal Role of miR-770 in Solid Tumors Carcinogenesis.Advanced biomedical research · 2026Review
- Mathematical models of intercellular signaling in breast cancer.Seminars in cancer biology · 2025Review
- Interdependency of estradiol-mediated ERα activation and subsequent PR and GREB1 induction to control cell cycle progression.Heliyon · 2024Article
- An evolutionary differential game for regulating the role of monoclonal antibodies in treating signalling pathways in oesophageal cancer.Royal Society open science · 2024Article
- Modeling of Mouse Experiments Suggests that Optimal Anti-Hormonal Treatment for Breast Cancer is Diet-Dependent.Bulletin of mathematical biology · 2024Article
- A robust optimal control framework for controlling aberrant RTK signaling pathways in esophageal cancer.Journal of mathematical biology · 2024Article
- Utilizing the Hippo pathway as a therapeutic target for combating endocrine-resistant breast cancer.Cancer cell international · 2021Review
- Personalized Medicine for Neuroblastoma: Moving from Static Genotypes to Dynamic Simulations of Drug Response.Journal of personalized medicine · 2021Review
- Mathematical modelling of breast cancer cells in response to endocrine therapy and Cdk4/6 inhibition.Journal of the Royal Society, Interface · 2020Article
- Systems biology: perspectives on multiscale modeling in research on endocrine-related cancers.Endocrine-related cancer · 2019Review
- Involvement of miR-770-5p in trastuzumab response in HER2 positive breast cancer cells.PloS one · 2019Article
- In Vivo Phosphoproteome Analysis Reveals Kinome Reprogramming in Hepatocellular Carcinoma.Molecular & cellular proteomics : MCP · 2018Article
- The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis.Nature communications · 2016Article
- Role of nuclear receptors in breast cancer stem cells.World journal of stem cells · 2016Review
- Endocrine resistance in breast cancer--An overview and update.Molecular and cellular endocrinology · 2015Review
- Sustained proliferation in cancer: Mechanisms and novel therapeutic targets.Seminars in cancer biology · 2015Review
- A kinetic model identifies phosphorylated estrogen receptor-α (ERα) as a critical regulator of ERα dynamics in breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Myeloid cell-derived inducible nitric oxide synthase suppresses M1 macrophage polarization.Nature communications · 2015Article
- Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers.Frontiers in oncology · 2015Review
- Mathematical models of the transitions between endocrine therapy responsive and resistant states in breast cancer.Journal of the Royal Society, Interface · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer cells develop resistance to endocrine therapies by shifting between estrogen receptor (ER)-regulated and growth factor receptor (GFR)-regulated survival signaling pathways. To study this switch, we propose a mathematical model of crosstalk between these pathways. The model explains why MCF7 sub-clones transfected with HER2 or EGFR show three GFR-distribution patterns, and why the bimodal distribution pattern can be reversibly modulated by estrogen. The model illustrates how transient overexpression of ER activates GFR signaling and promotes estrogen-independent growth. Understanding this survival-signaling switch can help in the design of future therapies to overcome resistance in breast cancer.
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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.