ArticleCell cycle (Georgetown, Tex.)2024
Thyroid hormone enhances estrogen-mediated proliferation and cell cycle regulatory pathways in steroid receptor-positive breast Cancer.
Article in Cell cycle (Georgetown, Tex.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Thyroid autoimmunity, thyroid function, and endometriosis: reproductive immune-endocrine crosstalk and causal uncertainty.Frontiers in medicine · 2026Review
- Development and validation of a multifactorial risk prediction model for breast cancer patients with co-occurring thyroid cancer: a retrospective matched case-control study.Frontiers in oncology · 2026Article
- MammOnc-DB, an integrative breast cancer data analysis platform for target discovery.NPJ breast cancer · 2025Article
- An investigation of the pattern and mechanism of comorbidity in patients with Hashimoto's thyroiditis.Frontiers in endocrinology · 2025Article
- Risk of Second Primary Cancer Among Patients with Thyroid Carcinoma in Finland: A Nationwide Population-Based Study.Clinical epidemiology · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
Estrogen receptor (ER) α expression and associated signaling is a major driver of over two-thirds of all breast cancers (BC). ER targeting strategies are typically used as a first-line therapy in patients with steroid receptor positive (SR+) disease. Secondary resistance to anti-estrogenic agents may occur with clonal expansion and disease progression. Mechanisms underlying hormone resistance are an expanding field of significant translational importance. Cross-talk with other nuclear hormones, receptors, and signaling pathways, including thyroid hormones (TH) and their receptors (THRs), have been shown to promote endocrine therapy resistance in some studies. We have shown that TH replacement therapy (THRT) was independently and significantly associated with higher rates of relapse and mortality in SR positive (+), node-negative (LN-) BC patients, whereas it showed no association with outcomes in SR negative (-) patients. LN-, SR+ patients receiving THRT and tamoxifen had the worst outcomes, suggesting a pro-carcinogenic interaction that significantly and independently shortened survival and increased mortality. Using
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