ArticleOncogene2011
Progression of BRAF-induced thyroid cancer is associated with epithelial-mesenchymal transition requiring concomitant MAP kinase and TGFβ signaling.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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.
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Who cites it
103 citing papers in PubMed, 169 citations in OpenAlex.
- Deciphering functional intra-tumoral heterogeneity in BRAFOncogene · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- NOX4-derived oxidative DNA damage impairs thyroid differentiation through an epigenetic mechanism in BRAF-mutated radioactive iodine refractory papillary thyroid cancer cells.International journal of biological sciences · 2026Article
- TGF-β1-based restoration of sodium iodide symporter expression in radioiodine-refractory differentiated thyroid cancer via engineered MSCs.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Mechanistic Aspects of Inflammation and Oxidative Stress and Their Association With Thyroid Cancer Risk.Cancer medicine · 2025Review
- Development of animal models to study aggressive thyroid cancers.European thyroid journal · 2025Review
- The regulatory network of epithelial-mesenchymal transition-associated non-coding RNAs in thyroid cancer: molecular mechanisms, clinical implications, and therapeutic strategies.Frontiers in oncology · 2025Review
- Modulating gene expression as a strategy to investigate thyroid cancer biology.Archives of endocrinology and metabolism · 2024Review
- Systemic treatments for radioiodine-refractory thyroid cancers.Frontiers in endocrinology · 2024Review
- TERT accelerates BRAF mutant-induced thyroid cancer dedifferentiation and progression by regulating ribosome biogenesis.Science advances · 2023Article
- Different Molecular Phenotypes of Progression in BRAF- and RAS-Like Papillary Thyroid Carcinoma.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- Deiodinases in thyroid tumorigenesis.Endocrine-related cancer · 2023Review
- Development of Novel Murine BRAFCancers · 2023Article
- β-catenin attenuation leads to up-regulation of activating NKG2D ligands and tumor regression inFrontiers in immunology · 2023Article
- Article
- Targeting non-canonical pathways as a strategy to modulate the sodium iodide symporter.Cell chemical biology · 2022Article
- Review
- Roles and new Insights of Macrophages in the Tumor Microenvironment of Thyroid Cancer.Frontiers in pharmacology · 2022Review
- Utility of droplet digital polymerase chain reaction for TERT and BRAF mutational profiling of thyroid nodules.BMC cancer · 2021Article
- Single-cell transcriptomic analysis of the tumor ecosystems underlying initiation and progression of papillary thyroid carcinoma.Nature communications · 2021Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Mice with thyroid-specific expression of oncogenic BRAF (Tg-Braf) develop papillary thyroid cancers (PTCs) that are locally invasive and have well-defined foci of poorly differentiated thyroid carcinoma (PDTC). To investigate the PTC-PDTC progression, we performed a microarray analysis using RNA from paired samples of PDTC and PTC collected from the same animals by laser capture microdissection. Analysis of eight paired samples revealed a profound deregulation of genes involved in cell adhesion and intracellular junctions, with changes consistent with an epithelial-mesenchymal transition (EMT). This was confirmed by immunohistochemistry, as vimentin expression was increased and E-cadherin lost in PDTC compared with adjacent PTC. Moreover, PDTC stained positively for phospho-Smad2, suggesting a role for transforming growth factor (TGF)β in mediating this process. Accordingly, TGFβ-induced EMT in primary cultures of thyroid cells from Tg-Braf mice, whereas wild-type thyroid cells retained their epithelial features. TGFβ-induced Smad2 phosphorylation, transcriptional activity and induction of EMT required mitogen-activated protein kinase (MAPK) pathway activation in Tg-Braf thyrocytes. Hence, tumor initiation by oncogenic BRAF renders thyroid cells susceptible to TGFβ-induced EMT, through a MAPK-dependent process.
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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.