Thyroid Gland Follicular Carcinoma

RET activation is a complex process involving multiple intracellular events, including calcium ion binding, glial cell line‑derived neurotrophic factor family ligand binding, and RET receptor aggregation, dimerization and autophosphorylation. The present study reviews the structure and function of the RET proto‑oncogene and its pathogenic roles in various TC subtypes.

Distinguishing FA with HTT-like morphology from genuine HTT might have therapeutic and prognostic (follow-up) implications, based on the benign nature of the former and the low-risk biology of the latter. However, the full biological spectrum of this FA subtype and its genetic background need more delineation in larger future studies with long follow-up.

This study shows that DMDTCs are characterized by dysregulated phosphorylation signalling, accompanied by chromosomal instability and aberrant methylation, thus underscoring DDR gene-targeted therapy as a promising strategy.

This case highlights the diagnostic challenge of perianal BCC mimicking benign lesions and emphasizes the need for histopathological confirmation. Follicular differentiation is exceptionally uncommon and should be distinguished from adnexal tumors such as trichoblastic carcinoma.

NTRK-fusion defines a distinct PTC molecular subtype characterized by a high burden of LNM and a spectrum of features linked to follicular growth patterns. These findings facilitate the preoperative identification of this tumor subtype and provide a foundation for individualized risk stratification and tailored management strategies.

PTEN alterations detected preoperatively confer an intermediate ROM (∼32%) in surgically followed cohorts, but ROM is modulated by pathway-related selection for surgery and by how PTEN alteration is operationalized (sequence variant vs protein loss). A PTEN-altered preoperative result should be communicated as a moderate-risk molecular finding that frequently maps to follicular/oncocytic neoplasia yet includes differentiated carcinomas and rare high-grade disease, supporting integrated pathology-radiology-molecular decision-making.

P2, N=40, Completed, Gustave Roussy, Cancer Campus, Grand Paris | Active, not recruiting --> Completed | Trial completion date: Dec 2022 --> Jan 2026

In vitro experiments further confirmed that, under inflammatory conditions, mast cells secreted IL-8, which activated the PI3K/AKT pathway and promoted malignant phenotypes. Collectively, these findings suggest that IL1B⁻ FECs recruit mast cells through the FN1/CD44 axis, and mast cell-derived IL-8 subsequently activates the PI3K/AKT pathway to drive the transformation from HT to PTC, providing novel mechanistic insights into the "inflammation-to-cancer" transition.

CD15 demonstrates high specificity for PTC. However, its limited sensitivity and variable expression in follicular-patterned lesions make its prognostic value unclear. CD15 should not be used as a standalone marker; instead, it may improve diagnostic accuracy when combined with other markers in multiparametric immunohistochemical panels.

P=N/A, N=50, Recruiting, M.D. Anderson Cancer Center | Initiation date: Feb 2026 --> Aug 2025

Co-occurring genetic alterations with RAS mutations markedly increased the risk of malignancy compared with isolated RAS mutations (Fisher's exact test, two-tailed p = 0.0026) and were associated with more aggressive tumor phenotypes, whereas isolated RAS mutations were more common in indolent neoplasms. Comprehensive molecular profiling is essential for accurate risk stratification and management of indeterminate thyroid nodules.

P4, N=50, Completed, Eisai Pharmaceuticals India Pvt. Ltd | Trial completion date: Apr 2025 --> Sep 2025 | Trial primary completion date: Apr 2025 --> Sep 2025 | Active, not recruiting --> Completed