ArticleOncotarget2011
Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors.
Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 82 citations in OpenAlex.
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- Cyclin C promotes pancreatic developmentand suppresses cancer initiation by maintenance of the autophagy-lysosome pathway.iScience · 2026Article
- The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026Review
- Dedifferentiation and Redifferentiation of Follicular-Cell-Derived Thyroid Carcinoma: Mechanisms and Therapeutic Implications.Biomedicines · 2025Review
- Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.European thyroid journal · 2025Review
- Review
- Developments in the study of the role of lactate metabolism in the genesis and progression of thyroid cancer.Frontiers in cell and developmental biology · 2025Review
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- Anaplastic thyroid cancer cells upregulate mitochondrial one-carbon metabolism to meet purine demand, eliciting a critical targetable vulnerability.Cancer letters · 2023Article
- Mechanistic Insights of Thyroid Cancer Progression.Endocrinology · 2023Review
- Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- Reducing the aneuploid cell burden - cell competition and the ribosome connection.Disease models & mechanisms · 2022Review
- Study on the Antitumor Effect and Glycolysis of Andrographolide in Anaplastic Thyroid Carcinoma.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Real-time, high-resolution imaging of tumor cells in genetically engineered and orthotopic models of thyroid cancer.Endocrine-related cancer · 2020Article
- Molecular therapeutics for anaplastic thyroid cancer.Seminars in cancer biology · 2020Article
- Mouse Model of Thyroid Cancer Progression and Dedifferentiation Driven by STRN-ALK Expression and Loss of p53: Evidence for the Existence of Two Types of Poorly Differentiated Carcinoma.Thyroid : official journal of the American Thyroid Association · 2019Article
- Synergistic repression of thyroid hyperplasia by cyclin C and Pten.Journal of cell science · 2019Article
- Comprehensive Genetic Characterization of Human Thyroid Cancer Cell Lines: A Validated Panel for Preclinical Studies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Anaplastic thyroid carcinoma (ATC) is the most aggressive form of thyroid cancer, and often derives from pre-existing well-differentiated tumors. Despite a relatively low prevalence, it accounts for a disproportionate number of thyroid cancer-related deaths, due to its resistance to any therapeutic approach. Here we describe the first mouse model of ATC, obtained by combining in the mouse thyroid follicular cells two molecular hallmarks of human ATC: activation of PI3K (via Pten deletion) and inactivation of p53. By 9 months of age, over 75% of the compound mutant mice develop aggressive, undifferentiated thyroid tumors that evolve from pre-existing follicular hyperplasia and carcinoma. These tumors display all the features of their human counterpart, including pleomorphism, epithelial-mesenchymal transition, aneuploidy, local invasion, and distant metastases. Expression profiling of the murine ATCs reveals a significant overlap with genes found deregulated in human ATC, including genes involved in mitosis control. Furthermore, similar to the human tumors, [Pten, p53]thyr-/- tumors and cells are highly glycolytic and remarkably sensitive to glycolysis inhibitors, which synergize with standard chemotherapy. Taken together, our results show that combined PI3K activation and p53 loss faithfully reproduce the development of thyroid anaplastic carcinomas, and provide a compelling rationale for targeting glycolysis to increase chemotherapy response in ATC 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.