Thyroid Gland Follicular Carcinoma

The analysis revealed an association between the BRAF V600E mutation and papillary thyroid cancer in patients exposed to radiation from nuclear testing at the former SNTS. These findings offer new prospects for targeted therapy and early diagnosis of malignant thyroid neoplasms. Following the closure of the test site, positive developments in public health have been observed: radiophobia has decreased and the population's quality of life has improved. Furthermore, the adoption of iodine prophylaxis legislation and the country's industrial growth have contributed to improved well-being and better epidemiological outcomes for thyroid cancer in subsequent generations.

Thus, the genomic profile of canine FTC differs significantly from that of humans, with limited reliance on RAS/RAF signaling for oncogenic progression. Conversely, RET signaling likely underlies tumorigenesis in both canine and human MTC.

Molecular testing in nodules ≥4 ​cm may underestimate malignancy risk. Clinicians should interpret benign MT results in this subgroup with caution.

In our small case series, no association was demonstrated between simultaneous MTC/PTC and age, CEA, calcitonin levels, gender, or number of operations. This entity likely represents a primary tumor with an incidental pathologic finding of a second malignancy.

The combination of high SUVmax, CT-detected calcification, and high thyroglobulin levels strongly suggests follicular carcinoma and may warrant resection.

Study limitations include its retrospective design, single-centre setting, and lack of inter-observer variability assessment. A risk-adapted multimodal surveillance strategy with 6-monthly US for two years is recommended.

An additional unique feature was an area demonstrating a "mixed" C-cell/thyroid follicular epithelial phenotype. In this review we review the possible etiologies of calcitonin-negative MTC, the possibility of a neoplastic sequential progression from ultimobranchial bodies to CCH/MMC to medullary thyroid carcinoma with the individual elements (UBB, CCH/MMC, MTC) demonstrated in this thyroid, and previous postulations that ultimobranchial bodies may be the source of some follicular thyroid cancers, medullary thyroid cancers, and mixed tumors of medullary and follicular epithelial types.

In conclusion, we found a lower TDS in malignant compared to benign thyroid neoplasms and demonstrated the prognostic role of TDS in differentiated tumors. These findings could preoperatively improve both the differential diagnosis of cytologically indeterminate nodules and the selection of the best surgical approach.

A model combining four miRNAs (miR-6085, miR-146b-5p, miR-221, and miR-222) demonstrated high sensitivity, specificity, and accuracy, suggesting that it could be a useful tool for differentiating FC from FA.

Furthermore, carbonic anhydrase 12 inhibitor U104 suppressed follicular thyroid carcinoma cell growth in a dose-dependent manner, and its combination with lenvatinib exerted synergistic antiproliferative effects. Collectively, these findings identified carbonic anhydrase 12 as a novel prognostic biomarker of follicular thyroid carcinoma and a promising therapeutic target.

Additionally, a FOXK1::GRHL1 fusion was found in the case of trichogerminoma. Clinical follow-up (15/16 patients; 94%; median: 65 months; range 2.5-106.5 months) showed no evidence of residual or metastatic disease.

Understanding the genetic landscape of thyroid carcinoma of follicular cells is essential to optimize clinical management and to identify molecular targets to treat cases with aggressive disease refractory to standard radioactive iodine therapy. What follows is a comprehensive and updated outline of the main somatic genetic and molecular alterations in thyroid carcinoma of follicular cells.