ArticleMolecular and cellular pharmacology2010
Epigenetic Reactivation of Estrogen Receptor: Promising Tools for Restoring Response to Endocrine Therapy.
Article in Molecular and cellular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04999540 (Trial of Tucidinostat in Combination With Fulvestrant in Patients With Hormone-receptor Positive Advanced Breast Cancer), which is not on this map. Cited by 17 papers, 3 of them syntheses that pooled it.
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.
Trial of Tucidinostat in Combination With Fulvestrant in Patients With Hormone-receptor Positive Advanced Breast Cancer
Who cites it
17 citing papers in PubMed, 3 syntheses or guidelines pooled it, 24 citations in OpenAlex.
- The Role of Estrogen Receptor-Targeted PET with 16α-Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026Pooled it
- Hormone, Targeted, and Combinational Therapies for Breast Cancers: From Humans to Dogs.International journal of molecular sciences · 2024Pooled it
- Overcoming resistance to endocrine therapy in hormone receptor-positive human epidermal growth factor receptor 2-negative (HRFrontiers of medicine · 2021Pooled it
- Entinostat, a class I selective histone deacetylase inhibitor, plus exemestane for Chinese patients with hormone receptor-positive advanced breast cancer: A multicenter, randomized, double-blind, placebo-controlled, phase 3 trial.Acta pharmaceutica Sinica. B · 2023Trial
- Epigenetic Therapeutics Targeting NRF2/KEAP1 Signaling in Cancer Oxidative Stress.Frontiers in pharmacology · 2022Review
- Molecular Mechanisms of Endocrine Resistance in Estrogen-Positive Breast Cancer.Frontiers in endocrinology · 2021Review
- Which Clinicopathologic Parameters Suggest Primary Resistance to Palbociclib in Combination With Letrozole as the First-Line Treatment for Hormone Receptor-Positive, HER2-Negative Advanced Breast Cancer?Frontiers in oncology · 2021Article
- Epigenetic Regulatory Mechanisms Induced by Resveratrol.Nutrients · 2017Review
- Article
- miRNAs involved in LY6K and estrogen receptor α contribute to tamoxifen-susceptibility in breast cancer.Oncotarget · 2016Article
- Article
- Therapeutic perspectives of epigenetically active nutrients.British journal of pharmacology · 2015Review
- Sulforaphane enhances Nrf2 expression in prostate cancer TRAMP C1 cells through epigenetic regulation.Biochemical pharmacology · 2013Article
- Mutant p53 binds to estrogen receptor negative promoter via DNMT1 and HDAC1 in MDA-MB-468 breast cancer cells.Molecular biology reports · 2013Article
- Derailed estrogen signaling and breast cancer: an authentic couple.Endocrine reviews · 2013Review
- Bioactive dietary supplements reactivate ER expression in ER-negative breast cancer cells by active chromatin modifications.PloS one · 2012Article
- PAX2 is activated by estradiol in breast cancer cells of the luminal subgroup selectively, to confer a low invasive phenotype.Molecular cancer · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Breast tumors expressing estrogen receptor alpha (ER) respond well to therapeutic strategies using SERMs (selective estrogen receptor modulators) such as tamoxifen. However, about thirty percent of invasive breast cancers are hormone independent because they lack ER expression due to hypermethylation of ER promoter. Treatment of ER-negative breast cancer cells with demethylating agents and histone deacetylase inhibitors leads to expression of ER mRNA and functional protein. Additionally, growth factor signaling pathways have also been implicated in ER silencing in ER-negative tumor phenotype. Recently, important role of components of ubiquitin-proteasome pathway has been shown in mediating downregulation of ER. In this article, we will review various mechanisms underlying the silencing of ER in ER negative tumor phenotype and discuss diverse strategies to combat it. Ongoing studies may provide the mechanistic insight to design therapeutic strategies directed towards epigenetic and non-epigenetic mechanisms in the prevention or treatment of ER-negative breast cancer.
Identifiers
21499573PMC3076694W1606938115What OpenQuestion holds
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.