ArticleProceedings of the National Academy of Sciences of the United States of America2011
Thyrotrophin receptor signaling dependence of Braf-induced thyroid tumor initiation in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 223 citations in OpenAlex.
- Dabrafenib and Trametinib Treatment in Patients With Locally Advanced or Metastatic BRAF V600-Mutant Anaplastic Thyroid Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Trial
- Hashimoto's thyroiditis influences tumor cell states and intratumoral microbiota in papillary thyroid carcinoma.iScience · 2026Article
- ERK Signaling in Thyroid Cancer: Lineage Suppression, Epigenetic Reprogramming, and Theranostic Reversal.Cancers · 2026Review
- Dynamic Predictors for Malignancy Risk of Follicular Thyroid Neoplasms: A Real-World, 10-Year Cohort Study.Cancer medicine · 2026Article
- The Role of Mitochondrial Genome Stability and Metabolic Plasticity in Thyroid Cancer.Biomedicines · 2025Review
- TET1 loss propels the development of hyperthyroidism by remodeling histone modifications of PAX8 promoter.Experimental & molecular medicine · 2025Article
- Tailoring TSH suppression in differentiated thyroid carcinoma: evidence, controversies, and future directions.Endocrine · 2025Review
- Tumor Cell Plasticity and Stromal Microenvironment Distinguish Papillary and Follicular Growth Patterns in a Mouse Model of BRAFV600E-Induced Thyroid Cancer.Cancer research communications · 2025Article
- Development of animal models to study aggressive thyroid cancers.European thyroid journal · 2025Review
- Reduced sensitivity to thyroid hormones is associated with differentiated thyroid cancer in the euthyroid thyroidectomy population.Frontiers in endocrinology · 2025Article
- Article
- Promising Therapeutic Targets for Recurrent/Metastatic Anaplastic Thyroid Cancer.Current treatment options in oncology · 2024Review
- Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis.Nature communications · 2024Article
- Targeting miR-31 represses tumourigenesis and dedifferentiation of BRAFClinical and translational medicine · 2024Article
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- Modulating gene expression as a strategy to investigate thyroid cancer biology.Archives of endocrinology and metabolism · 2024Review
- METTL3 regulates thyroid cancer differentiation and chemosensitivity by modulating PAX8.International journal of biological sciences · 2024Article
- Activation of mitogen-activated protein kinase signaling and development of papillary thyroid carcinoma in thyroid-stimulating hormone receptor D633H knockin mice.European thyroid journal · 2023Article
- Telomerase Upregulation Induces Progression of Mouse BrafV600E-Driven Thyroid Cancers and Triggers Nontelomeric Effects.Molecular cancer research : MCR · 2023Article
- Review
72 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
Mutations of BRAF are found in ∼45% of papillary thyroid cancers and are enriched in tumors with more aggressive properties. We developed mice with a thyroid-specific knock-in of oncogenic Braf (LSL-Braf(V600E)/TPO-Cre) to explore the role of endogenous expression of this oncoprotein on tumor initiation and progression. In contrast to other Braf-induced mouse models of tumorigenesis (i.e., melanomas and lung), in which knock-in of Braf(V600E) induces mostly benign lesions, Braf-expressing thyrocytes become transformed and progress to invasive carcinomas with a very short latency, a process that is dampened by treatment with an allosteric MEK inhibitor. These mice also become profoundly hypothyroid due to deregulation of genes involved in thyroid hormone biosynthesis and consequently have high TSH levels. To determine whether TSH signaling cooperates with oncogenic Braf in this process, we first crossed LSL-Braf(V600E)/TPO-Cre with TshR knockout mice. Although oncogenic Braf was appropriately activated in thyroid follicular cells of these mice, they had a lower mitotic index and were not transformed. Thyroid-specific deletion of the Gsα gene in LSL-Braf(V600E)/TPO-Cre/Gnas-E1(fl/fl) mice also resulted in an attenuated cancer phenotype, indicating that the cooperation of TshR with oncogenic Braf is mediated in part by cAMP signaling. Once tumors were established in mice with wild-type TshR, suppression of TSH did not revert the phenotype. These data demonstrate the key role of TSH signaling in Braf-induced papillary thyroid cancer initiation and provide experimental support for recent observations in humans pointing to a strong association between TSH levels and thyroid cancer incidence.
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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.