Loading
Thyroid Cancer Diagnosis and Treatment / Clusterin in Disease Pathology · Journal article
European Thyroid Journal · September 9, 2026
A consensus or society position rather than new primary data.
This is a narrative review consolidating evidence that TERT promoter mutations (c.-124C>T and c.-146C>T) are independent predictors of aggressive behaviour, radioiodine refractoriness, and poor survival in thyroid cancer, with particular risk when co-occurring with BRAFV600E. The review identifies telomerase and ribosome-targeted inhibitors (Imetelstat, CX5461) as emerging therapeutic options supported by preclinical data, and recommends TERT mutation status for clinical risk stratification.
Narrative review. Patients with thyroid cancer (papillary, anaplastic, and refractory disease).
TERT c.-124C>T and c.-146C>T hotspot mutations discovered in 2013 are independent predictors of disease-specific survival, recurrence and radioiodine refractoriness. TERT promoter mutations increase in prevalence from papillary to anaplastic thyroid carcinoma. Co-occurrence of TERT promoter mutations with BRAFV600E substantially increases risk of radioiodine-refractory disease.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should consider TERT promoter mutation status in risk stratification and prognosis discussion, with particular attention to molecular context (co-mutations with BRAFV600E). Emerging telomerase- and ribosome-targeted agents may offer therapeutic options for TERT-driven or radioiodine-refractory thyroid cancers, though clinical trial evidence is not yet reported here.
A narrative review synthesizing mechanistic understanding and clinical evidence on TERT mutations in thyroid cancer, with expert consensus on risk stratification and emerging therapeutic strategies, but not a primary data study.
As stated by the source record.
Clinicians should consider TERT promoter mutation status in risk stratification and prognosis discussion, with particular attention to molecular context (co-mutations with BRAFV600E). Emerging telomerase- and ribosome-targeted agents may offer therapeutic options for TERT-driven or radioiodine-refractory thyroid cancers, though clinical trial evidence is not yet reported here.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Abstract Somatic mutations in the Telomerase reverse transcriptase (TERT) promoter are key molecular events in thyroid carcinogenesis and are strongly associated with aggressive clinical behaviour. The c.-124C>T and c.-146C>T hotspot mutations, discovered in 2013, are now recognised as major mechanisms of TERT reactivation and as independent predictors of disease-specific survival, recurrence and disease refractoriness to radioiodine. TERT can also be reactivated by multiple regulatory layers converging on telomerase upregulation. Beyond telomere maintenance, TERT enhances ribosome biogenesis, cooperates with BRAFV600E-driven transcriptional programmes and modulates NF-κB-associated inflammatory and stress responses, thereby promoting dedifferentiation and therapy resistance. Clinically, TERT promoter mutations, particularly when co-occurring with BRAFV600E, increase in prevalence from papillary to anaplastic thyroid carcinoma and are associated with an increased risk of radioiodine-refractory disease, supporting their use in risk stratification. However, isolated TERT promoter mutations are more often associated with intermediate risk tumours and comparatively better outcomes, underscoring the importance of molecular context. The recent approval of the telomerase inhibitor Imetelstat and the preclinical success of the rRNA transcription inhibitor CX5461 in restoring differentiation and iodine uptake support telomerase- and ribosome-targeted strategies as emerging therapeutic avenues for TERT-driven thyroid cancers.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.