BRAF V600E

P1/2, N=101, Completed, Erasca, Inc. | Active, not recruiting --> Completed

P2/3, N=94, Recruiting, Centre Hospitalier Regional Universitaire | Not yet recruiting --> Recruiting

P2, N=25, Recruiting, Vall d'Hebron Institute of Oncology | Not yet recruiting --> Recruiting

P2, N=10, Active, not recruiting, UNICANCER | Trial completion date: Apr 2029 --> Mar 2026 | Trial primary completion date: Apr 2025 --> Mar 2026

Only one patient died 16 months after surgery due to an unrelated traffic accident.

We developed and validated an XGBoost-based machine learning model that accurately predicts high-risk distant metastatic recurrence in DTC patients. This model may help clinicians identify patients who could benefit from more aggressive treatment and intensive follow-up, enabling personalized management strategies.

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.

It suggests that neoplastic compression should be suspected in male patients with recurrent CTS, especially when preoperative imaging is negative, and meticulous intraoperative exploration is crucial. Literature analysis shows that wrist tumors are prone to recurrent nerve compression due to anatomical space limitations, and early identification followed by surgical resection is key to improving prognosis.

The vemurafenib combined with 131I revealed superior efficacy in improving survival and thyroid function recovery in lymph node metastatic BRAF-mutant thyroid cancer.

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.

This functional inhibition persists following DNA damage or pharmacologic disruption of TP53 pathways, demonstrating that oncogenic BRAF constrains TP53 activity. These findings establish a protein interaction through which BRAFV600E functionally inactivates TP53 and reveal a mechanism by which melanoma bypasses TP53-mediated tumor suppression without requiring genetic alteration.