ArticleThe Journal of clinical investigation2016
Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 731 papers, 8 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
731 citing papers in PubMed, 8 syntheses or guidelines pooled it, 1,248 citations in OpenAlex.
- Korean Thyroid Association Guidelines on the Management of Differentiated Thyroid Cancers, Part II: Follow-up Surveillance after Initial Treatment 2026.Endocrinology and metabolism (Seoul, Korea) · 2026Guideline
- 2025 American Thyroid Association Management Guidelines for Adult Patients with Differentiated Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2025Guideline
- Aggressive Thyroid Carcinomas Clinical and Molecular Features: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- The 2024 revised clinical guidelines on the management of thyroid tumors by the Japan Association of Endocrine Surgery.Endocrine journal · 2025Guideline
- Rationale for Testing TP53 Mutations in Thyroid Cancer-Original Data and Meta-Analysis.International journal of molecular sciences · 2025Pooled it
- Emerging insights into thyroid cancer from immunotherapy perspective: A bibliometric analysis.Human vaccines & immunotherapeutics · 2024Pooled it
- SEOM-GETNE-TTCC Clinical guideline thyroid cancer (2023).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Guideline
- Current evidences in poorly differentiated thyroid carcinoma: a systematic review and subsection meta-analysis for clinical decision making.Endocrine · 2024Pooled it
- Single-cell sequencing profiling of intratumoral heterogeneity and immunosuppressive microenvironment in primary thyroid cancer and lymph node metastases.Oncoimmunology · 2026Article
- Durable response of anaplastic thyroid cancer to pembrolizumab combined with chemotherapy: A case report.Human vaccines & immunotherapeutics · 2026Article
- From bench to bedside: the evolving role of iodine in thyroid cancer management.Nature reviews. Endocrinology · 2026Review
- Signaling pathways and targeted therapy in high‑risk refractory thyroid cancer: From bench to bedside (Review).International journal of oncology · 2026Review
- EIF1AX Mutations in thyroid nodules and advanced thyroid carcinoma: a systematic review and meta-analysis.Virchows Archiv : an international journal of pathology · 2026Review
- Latin American Thyroid Society expert panel consensus on anaplastic thyroid cancer.Archives of endocrinology and metabolism · 2026Article
- Synergistic role of molecular imaging and genomics in thyroid cancer management: from diagnosis to personalized treatment.Journal of translational medicine · 2026Review
- Single-Cell Transcriptome of Anaplastic Thyroid Cancer Reveals Immunosuppressive Tumor Microenvironment Remodeling.Cancer medicine · 2026Article
- SMARCA4-deficient Anaplastic Thyroid Carcinoma: A Hitherto Unreported Case.Virchows Archiv : an international journal of pathology · 2026Article
- Anaplastic thyroid cancer: genomic landscape, molecular drivers and novel therapeutics.Nature reviews. Endocrinology · 2026Review
- ERK Signaling in Thyroid Cancer: Lineage Suppression, Epigenetic Reprogramming, and Theranostic Reversal.Cancers · 2026Review
- Genomics and Multi-Omics to Guide Clinical Management in Thyroid Cancer.International journal of molecular sciences · 2026Review
671 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
17 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPoorly differentiated thyroid cancer (PDTC) and anaplastic thyroid cancer (ATC) are rare and frequently lethal tumors that so far have not been subjected to comprehensive genetic characterization.
methodsWe performed next-generation sequencing of 341 cancer genes from 117 patient-derived PDTCs and ATCs and analyzed the transcriptome of a representative subset of 37 tumors. Results were analyzed in the context of The Cancer Genome Atlas study (TCGA study) of papillary thyroid cancers (PTC).
resultsCompared to PDTCs, ATCs had a greater mutation burden, including a higher frequency of mutations in TP53, TERT promoter, PI3K/AKT/mTOR pathway effectors, SWI/SNF subunits, and histone methyltransferases. BRAF and RAS were the predominant drivers and dictated distinct tropism for nodal versus distant metastases in PDTC. RAS and BRAF sharply distinguished between PDTCs defined by the Turin (PDTC-Turin) versus MSKCC (PDTC-MSK) criteria, respectively. Mutations of EIF1AX, a component of the translational preinitiation complex, were markedly enriched in PDTCs and ATCs and had a striking pattern of co-occurrence with RAS mutations. While TERT promoter mutations were rare and subclonal in PTCs, they were clonal and highly prevalent in advanced cancers. Application of the TCGA-derived BRAF-RAS score (a measure of MAPK transcriptional output) revealed a preserved relationship with BRAF/RAS mutation in PDTCs, whereas ATCs were BRAF-like irrespective of driver mutation.
conclusionsThese data support a model of tumorigenesis whereby PDTCs and ATCs arise from well-differentiated tumors through the accumulation of key additional genetic abnormalities, many of which have prognostic and possible therapeutic relevance. The widespread genomic disruptions in ATC compared with PDTC underscore their greater virulence and higher mortality.
fundingThis work was supported in part by NIH grants CA50706, CA72597, P50-CA72012, P30-CA008748, and 5T32-CA160001; the Lefkovsky Family Foundation; the Society of Memorial Sloan Kettering; the Byrne fund; and Cycle for Survival.
Indexed as
Identifiers
What OpenQuestion holds
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.