ArticleOncogene2016
TSH overcomes Braf(V600E)-induced senescence to promote tumor progression via downregulation of p53 expression in papillary thyroid cancer.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 57 citations in OpenAlex.
- The secreted protein SPARCL1 suppresses tumor progression in papillary thyroid carcinoma via SLC3A2-mediated ferroptosis.Endocrine-related cancer · 2026Article
- TSH suppression therapy from an individualized perspective: from mechanism to clinical decision-making.Frontiers in endocrinology · 2026Review
- Hashimoto's thyroiditis both promotes and protects against papillary thyroid cancer.Frontiers in endocrinology · 2026Review
- Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.European thyroid journal · 2025Review
- Tailoring TSH suppression in differentiated thyroid carcinoma: evidence, controversies, and future directions.Endocrine · 2025Review
- NOVEL INSIGHTS IN ADVANCED THYROID CARCINOMA: FROM MECHANISMS TO TREATMENTS: Molecular insights into the origin, biology, and treatment of anaplastic thyroid carcinoma.European thyroid journal · 2025Review
- Thyroid-Stimulating Hormone: An Important Target for the Prevention of Nonalcoholic Fatty Liver Disease.Physiological research · 2025Review
- Mutational Landmarks in Anaplastic Thyroid Cancer: A Perspective of a New Treatment Strategy.Journal of clinical medicine · 2025Review
- Cell membrane-derived nanovesicles as extracellular vesicle-mimetics in wound healing.Materials today. Bio · 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
- Identification of novel prognostic biomarkers for thyroid cancer by integrated transcriptome analysis of metastasis-associated genes.Frontiers in oncology · 2025Article
- Papillary thyroid carcinoma with Hashimoto's thyroiditis: impact and correlation.Frontiers in endocrinology · 2025Review
- Genome-wide transcriptome analysis and drug target discovery reveal key genes and pathways in thyroid cancer metastasis.Frontiers in endocrinology · 2025Article
- FBXO2 promotes the progression of papillary thyroid carcinoma through the p53 pathway.Scientific reports · 2024Article
- Association between Thyroid Profile Levels and Lymph Node Metastasis in Papillary Thyroid Carcinoma: A Retrospective Study.Reports (MDPI) · 2024Article
- Comprehensive analysis of cellular senescence and immune microenvironment in papillary thyroid carcinoma.Aging · 2024Article
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- Diabetes Mellitus and Thyroid Cancers: Risky Correlation, Underlying Mechanisms and Clinical Prevention.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- A review of complex hormone regulation in thyroid cancer: novel insights beyond the hypothalamus-pituitary-thyroid axis.Frontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
The BRAF(V600E) mutation is found in approximately 40% of papillary thyroid cancers (PTC). Mice with thyroid-specific expression of Braf(V600E) (TPO-Braf(V600E)) develop PTC rapidly with high levels of serum thyroid-stimulating hormone (TSH). It is unclear to what extent the elevated TSH contributes to tumor progression. To investigate the progression of Braf(V600E)-induced PTC (BVE-PTC) under normal TSH, we transplanted BVE-PTC tumors subcutaneously into nude and TPO-Braf(WT) mice. Regression of the transplanted tumors was observed in both nude and TPO-Braf(WT) mice. They were surrounded by heavy lymphocyte infiltration and oncogene-induced senescence (OIS) was demonstrated by strong β-gal staining and absence of Ki-67 expression. In contrast, BVE-PTC transplants continued to grow when transplanted into TPO-Braf(V600E) mice. The expression of Trp53 was increased in tumor transplants undergoing OIS. Trp53 inactivation reversed OIS and enabled tumor transplants to grow in nude mice with characteristic cell morphology of anaplastic thyroid cancer (ATC). PTC-to-ATC transformation was also observed in primary BVE-PTC tumors. ATC cells derived from Trp53 knockout tumors had increased PI3K/AKT signaling and became resistant to Braf(V600E) inhibitor PLX4720, which could be overcome by combined treatment of PI3K inhibitor LY294002 and PLX4720. In conclusion, BVE-PTC progression could be contained via p53-dependent OIS and TSH is a major disruptor of this balance. Simultaneous targeting of both MAPK and PI3K/AKT pathways offer a better therapeutic outcome against ATC. The current study reinforces the importance of rigorous control of serum TSH in PTC patients.
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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.