ReviewGenes2019
Molecular Alterations in Thyroid Cancer: From Bench to Clinical Practice.
Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis 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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Size Increment During Surveillance in Papillary Thyroid Cancer: Evidence Synthesis and Dose-Response Meta-Analysis.Cancer reports (Hoboken, N.J.) · 2025Pooled it
- Dabrafenib plus trametinib in patients with BRAF V600E-mutant anaplastic thyroid cancer: updated analysis from the phase II ROAR basket study.Annals of oncology : official journal of the European Society for Medical Oncology · 2022Trial
- Trial
- Article
- State of the Art on Thyroid Cancer Biology and Oncology.Biomedicines · 2026Review
- Hyperfunctioning distant metastases in high-grade differentiated thyroid carcinoma arising from HRAS-mutated follicular thyroid carcinoma: a case report and literature review.Frontiers in endocrinology · 2026Review
- The CHK1 inhibitor Prexasertib is effective againstFrontiers in endocrinology · 2026Article
- Functionalized nanomedicines for co-targeting of multiple pathways to efficiently treat thyroid cancer: prospects and challenges.Frontiers in pharmacology · 2026Review
- Molecular Diagnostics and Personalized Therapeutics in Differentiated Thyroid Carcinoma: A Clinically Oriented Review.Diagnostics (Basel, Switzerland) · 2025Review
- Advances in lenvatinib monotherapy and combination therapies in anaplastic thyroid cancer (Review).Oncology letters · 2025Review
- Proteomics profile in encapsulated follicular patterned thyroid neoplasms.Scientific reports · 2024Article
- Systemic treatments for radioiodine-refractory thyroid cancers.Frontiers in endocrinology · 2024Review
- Harnessing Immunity to Treat Advanced Thyroid Cancer.Vaccines · 2023Review
- Single-Cell Analysis in theGenes · 2023Review
- Clinical Implications of mTOR Expression in Papillary Thyroid Cancer-A Systematic Review.Cancers · 2023Review
- Cabozantinib, Vandetanib, Pralsetinib and Selpercatinib as Treatment for Progressed Medullary Thyroid Cancer with a Main Focus on Hypertension as Adverse Effect.International journal of molecular sciences · 2023Review
- How doFrontiers in endocrinology · 2023Article
- Combined expression of theGland surgery · 2022Article
- Epidermal growth factor receptor activation confers resistance to lenvatinib in thyroid cancer cells.Cancer science · 2022Article
- Strategies for Radioiodine Treatment: What's New.Cancers · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid cancer comprises different clinical and histological entities. Whereas differentiated (DTCs) malignancies are sensitive to radioiodine therapy, anaplastic (ATCs) and medullary (MTCs) tumors do not uptake radioactive iodine and display aggressive features associated with a poor prognosis. Moreover, in a majority of DTCs, disease evolution leads to the progressive loss of iodine sensitivity. Hence, iodine-refractory DTCs, along with ATCs and MTCs, require alternative treatments reflective of their different tumor biology. In the last decade, the molecular mechanisms promoting thyroid cancer development and progression have been extensively studied. This has led to a better understanding of the genomic landscape, displayed by thyroid malignancies, and to the identification of novel therapeutic targets. Indeed, several pharmacological compounds have been developed for iodine-refractory tumors, with four multi-target tyrosine kinase inhibitors already available for DTCs (sorafenib and lenvatinib) and MTCs (cabozantib and vandetanib), and a plethora of drugs currently being evaluated in clinical trials. In this review, we will describe the genomic alterations and biological processes intertwined with thyroid cancer development, also providing a thorough overview of targeted drugs already tested or under investigation for these tumors. Furthermore, given the existing preclinical evidence, we will briefly discuss the potential role of immunotherapy as an additional therapeutic strategy for the treatment of thyroid cancer.
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.