ReviewHormones & cancer2015
Recurrence of differentiated thyroid carcinoma during full TSH suppression: is the tumor now thyroid hormone dependent?
Review in Hormones & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- An overall and dose-response meta-analysis for thyrotropin and thyroid cancer risk by histological type.Oncotarget · 2016Pooled it
- Review
- Physiological Role and Use of Thyroid Hormone Metabolites - Potential Utility in COVID-19 Patients.Frontiers in endocrinology · 2021Review
- Actions of Thyroid Hormones on Thyroid Cancers.Frontiers in endocrinology · 2021Review
- The Thyroid Tumor Microenvironment: Potential Targets for Therapeutic Intervention and Prognostication.Hormones & cancer · 2020Review
- Review
- Molecular Functions of Thyroid Hormone Signaling in Regulation of Cancer Progression and Anti-Apoptosis.International journal of molecular sciences · 2019Review
- Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β.Molecular carcinogenesis · 2017Article
- Nongenomic actions of thyroid hormone.Nature reviews. Endocrinology · 2016Review
- Overlapping nongenomic and genomic actions of thyroid hormone and steroids.Best practice & research. Clinical endocrinology & metabolism · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Well-standardized primary treatment and long-term management of differentiated thyroid carcinoma (DTC) include lowering or suppression of host thyrotropin (TSH) with exogenous L-thyroxine (T4). This treatment recognizes the trophic action of TSH on DTC cells. Suppression of endogenous TSH with T4 is continued in recurrent disease. However, T4 can induce proliferation of follicular and papillary thyroid carcinoma cell lines and of other human carcinoma cells. The proliferative mechanism is initiated at a cell surface receptor for T4 on integrin αvβ3, a receptor by which the hormone also inhibits p53-dependent apoptosis in tumor cells. In recurrent DTC with satisfactory suppression of endogenous TSH, we discuss here the possibility that the tumor is no longer TSH dependent and that T4 has become a critical growth factor for the 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.