ArticleSeminars in cancer biology2020
Molecular therapeutics for anaplastic thyroid cancer.
Article in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- The NAT10/c-Myc positive feedback loop orchestrates tRNA acCellular & molecular biology letters · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- Article
- Review
- Post-translational modifications in anaplastic thyroid carcinoma: biological mechanisms and therapeutic potential.Cancer cell international · 2025Review
- Extracellular vesicle-associated transcriptomic and proteomic biomarkers show in vitro potential for vandetanib treatment monitoring in anaplastic thyroid cancer.Scientific reports · 2025Article
- Cross-tissue transcriptome-wide analysis reveals novel insights into thyroid cancer etiology.Discover oncology · 2025Article
- Epigenomic Modulators and Thyroid Hormone Receptor β Agonists: A New Paradigm for Tumor Suppression in Thyroid Cancer.Endocrinology · 2025Review
- Combination therapy of TKIs and ICIs for the treatment of anaplastic thyroid carcinoma.Frontiers in oncology · 2025Article
- Erianin induces apoptosis and pyroptosis via MAPK/ERK and PI3K/Akt pathways and synergizes with anlotinib in anaplastic thyroid carcinoma.Frontiers in pharmacology · 2025Article
- New Horizons of Biomarkers in Metastatic Thyroid Cancer.Journal of Cancer · 2025Review
- An Overview on Prevalence and Detection Approaches of BRAF V600E Mutation in Anaplastic Thyroid Carcinoma: A Systematic Review and Meta-Analysis.Iranian journal of public health · 2024Review
- Brusatol attenuated proliferation and invasion induced by KRAS in differentiated thyroid cancer through inhibiting Nrf2.Journal of endocrinological investigation · 2024Article
- Review
- miR-331-5p Affects Motility of Thyroid Cancer Cell Lines and Regulates BID Expression.Biomedicines · 2024Article
- TRβ Agonism Induces Tumor Suppression and Enhances Drug Efficacy in Anaplastic Thyroid Cancer in Female Mice.Endocrinology · 2023Article
- Pathogenic Insights into DNA Mismatch Repair (MMR) Genes-Proteins and Microsatellite Instability: Focus on Adrenocortical Carcinoma and Beyond.Diagnostics (Basel, Switzerland) · 2023Review
- Efficacy of anlotinib combined with radioiodine to treat scalp metastasis of papillary thyroid cancer: A case report and review of literature.World journal of clinical cases · 2023Article
- RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex.Cell & bioscience · 2023Article
- BI-847325, a selective dual MEK and Aurora kinases inhibitor, reduces aggressive behavior of anaplastic thyroid carcinoma on an in vitro three-dimensional culture.Cancer cell international · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Anaplastic thyroid cancer (ATC) represents one of the most lethal human cancers and although this tumor type is rare, ATC accounts for the majority of deaths from thyroid cancer. Due to the rarity of ATC, a comprehensive genomic characterization of this tumor type has been challenging, and thus the development of new therapies has been lacking. To date, there is only one mutation-driven targeted therapy for BRAF-mutant ATC. Recent genomic studies have used next generation sequencing to define the genetic landscape of ATC in order to identify new therapeutic targets. Together, these studies have confirmed the role of oncogenic mutations of MAPK pathway as key drivers of differentiated thyroid cancer (BRAF, RAS), and that additional genetic alterations in the PI3K pathway, TP53, and the TERT promoter are necessary for anaplastic transformation. Recent novel findings have linked the high mutational burden associated with ATC with mutations in the Mismatch Repair (MMR) pathway and overactivity of the AID/APOBEC family of cytidine deaminases. Additional novel mutations include cell cycle genes, SWI/SNF chromatin remodeling complex, and histone modification genes. Mutations in RAC1 were also identified in ATC, which have important implications for BRAF-directed therapies. In this review, we summarize these novel findings and the new genetic landscape of ATC. We further discuss the development of therapies targeting these pathways that are being tested in clinical and preclinical studies.
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