Brain Cancer

P=N/A, N=58, Active, not recruiting, Wake Forest University Health Sciences | Recruiting --> Active, not recruiting | N=244 --> 58

P1, N=40, Active, not recruiting, Iovance Biotherapeutics, Inc. | Recruiting --> Active, not recruiting

P=N/A, N=176, Recruiting, University Hospital, Essen | Not yet recruiting --> Recruiting

P2, N=38, Recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

P3, N=220, Recruiting, Sun Yat-sen University | Not yet recruiting --> Recruiting

P=N/A, N=20, Not yet recruiting, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins

This study provides genetic and functional evidence linking breast cancer to meningioma risk through DNA repair and hormonal pathways, supporting early risk assessment and targeted therapies to improve patient outcomes.

The diagnosis could only be established based on the DNA methylation profiling result. In light of these distinctive molecular findings, we propose some insights into the current WHO diagnostic criteria for DHG H3-G34 and emphasise the value of comprehensive molecular diagnosis.

Primary leiomyoma of the anterior mediastinum is extremely rare. Because primary mediastinal leiomyomas have nonspecific imaging features, distinguishing them from other anterior mediastinal tumors is challenging; thus, surgical resection is required for both diagnosis and treatment. Compared with the conventional look-up method, the confronting upside-down VATS technique utilizes higher intercostal access to provide a comprehensive thoracic view while minimizing diaphragmatic interference. The 180-degree rotated assistant monitor allows both surgeon and assistant to share a thoracotomy-like visual field, enhancing intraoperative coordination. In this case, it facilitated a stable operative field and phrenic nerve preservation despite the tumor's proximity without diaphragmatic interference. The confronting upside-down VATS technique may be particularly advantageous for anterior mediastinal tumors located along the phrenic nerve and in close proximity to the diaphragm.

In conclusion, SIX5 functions as a critical oncogenic driver in GBM, regulated by KDM5C and promoting tumor progression through UBE2C-mediated activation of AKT/mTOR signaling and glycolytic reprogramming. The KDM5C-SIX5-UBE2C regulatory axis represents a potential prognostic biomarker and therapeutic target in glioblastoma.

Conclusions Due to their rarity, these tumors may be overlooked in clinical practice. The low availability of diagnostic tests in many centers may contribute to the underestimation of the incidence of SFTs.

These combined actions lead to cell cycle arrest and mitotic catastrophe. Our findings establish Z5 as a promising clinical candidate for classical GBM, employing a unique dual mechanism that overcomes EGFR-targeted and DNA-damaging therapy limitations by synergistically targeting DNA and EGFR with high efficacy, advancing understanding of EGFR-WEE1 biology, and supporting clinical development.