P=N/A, N=142, Not yet recruiting, University of Michigan Rogel Cancer Center | Trial completion date: Apr 2029 --> Aug 2029 | Initiation date: Apr 2026 --> Aug 2026 | Trial primary completion date: Apr 2029 --> Aug 2029
1 day ago
Trial completion date • Trial initiation date • Trial primary completion date
BRAFV600E and TERT promoter co-mutation, identifiable preoperatively, defines a distinct PTC subtype with a profoundly aggressive clinicopathological profile and a significantly elevated risk of recurrence. This combined molecular signature is a potent preoperative biomarker for stratifying patients into the highest-risk category, potentially guiding more individualized initial therapeutic strategies.
BRAF mutation is presumed to be associated with tumor progression and may predict growth of PTMC. Genetic testing including BRAF testing may help distinguishing rapid-growing thyroid cancer.
Compared with the detection of either marker alone, the combined detection of Ctn and CEA improved the diagnostic accuracy for MTC but did not enhance the PPV. The combined detection also improved the predictive accuracy for cervical and lateral lymph node metastases and disease recurrence.
PD-L1 is a robust biomarker of aggressiveness in PTC. Integrating PD-L1 testing with molecular profiling can enhance postoperative risk stratification and guide personalized management.
P=N/A, N=5, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027
3 days ago
Trial completion date • Trial primary completion date
The approach emphasizes (i) selecting a thyroid-appropriate molecular assay from the outset whenever feasible, (ii) explicitly documenting residual suspicion and the scope of the performed assay in pathology reports, (iii) using pan-TRK immunohistochemistry only as an optional triage tool rather than a rule-out test, and (iv) considering RNA-based or other fusion-optimized assays only when the original clinical question remains unresolved and the result is clinically relevant. This framework is intended to reduce false reassurance from negative limited panels while reinforcing the need for appropriate molecular testing in the correct clinical scenario.
Selpercatinib, a RET inhibitor, is covered by insurance for all solid tumors that are positive for the RET fusion gene...In other solid tumors, positivity is less than 0.5%. However, if positive, treatment is expected to be effective, so it is desirable to actively perform cancer gene panel testing.
Pipette mixing of FNAC samples improves the detection efficiency of BRAF V600E mutation and enhances diagnostic accuracy for thyroid nodules, especially in challenging cases. This simple technique may optimize preoperative diagnosis and guide clinical decision-making.
RFA is a safe, useful, valuable, minimally invasive procedure, especially for small residual thyroid nodules post-thyroidectomy. Further research and trials are needed to establish the applicability and long-term effectiveness of the RFA.
Initial in vitro validation in a single RAIR-high/ATC-like thyroid cancer model provided proof-of-concept support for these predictions, with sorafenib showing dose-dependent cytotoxicity and suppression of RAF-MAPK signalling. A module-based RAIR signature captures a disease-focused component of a broader RAIR-ATC axis, transfers to cell-line models and can be embedded into an interpretable multimodal framework for drug-response prediction and targeted drug-class prioritisation, prioritising VEGFR/KDR and RAF/BRAF inhibitor classes as candidates for further translational evaluation in RAIR-like thyroid models.
The clinical course was marked by immune-triggered relapses and the patient responded well to intravenous immunoglobulin (IVIg) and FcRn inhibition with efgartigimod...This case illustrates a rare concurrence of relapsing AIDP, Graves' disease, and papillary thyroid carcinoma, and supports the hypothesis that persistent systemic immune activation underlies relapsing GBS, rather than a chronic demyelinating process. Clinically, it highlights the importance of considering underlying autoimmune and neoplastic conditions in atypical or relapsing GBS to guide individualized management.