Meningioma

Moreover, the GBM tumor microenvironment (TME) is enriched in arachidonic acid (AA)-derived cyclooxygenase (COX) products prostaglandins (PG) E2 and F2α in combination with enhanced CD24 expression. By our comparative approach, the data hint toward a pro-tumorigenic Siglec10+CX3CR1+ macrophage population depending on the characteristic tumor microenvironment (TME) of highly malignant GBMs.

P2, N=30, Not yet recruiting, Jazz Pharmaceuticals

Overall, we present a molecular targeting strategy for meningiomas that could pave the way for less invasive clinical management of these tumours and, as a result, help reduce patient mortality and morbidity. Metformin and sulforaphane both have FDA and EU pharmaceutical approval and thus could be repurposed promptly to establish a new meningioma therapy regimen.

P1/2, N=25, Recruiting, Fundación de investigación HM | Phase classification: P2 --> P1/2

Despite these advances, challenges remain, particularly in the standardization of classification systems, development of predictive biomarkers and optimization of trial designs. In this comprehensive, state-of-the-art Review we provide an integrated roadmap for meningioma care as well as a framework for ongoing and future research in this field.

P1/2, N=65, Recruiting, Nationwide Children's Hospital | Trial completion date: Nov 2027 --> Nov 2033 | Trial primary completion date: Nov 2027 --> Nov 2028

SRS presents as a reasonable primary option or should be considered for early intervention after surgery. Patients and families should be counseled that multiple SRS sessions might be needed to achieve eventual tumor control.

We report a rare case of dedifferentiated chondrosarcoma of the cavernous sinus in a specimen containing only the dedifferentiated component and exhibiting an IDH1 mutation, underscoring the importance of genetic characterization for the differential diagnosis of tumors in this anatomical region. Given the recent evidence supporting the efficacy of IDH inhibitors in chondrosarcomas, identifying mutations in these genes may also have significant therapeutic implications.

As evidence grows, SSTR PET may also provide insights into prognosis, with uptake patterns potentially correlating with recurrence risk and treatment response. Two illustrative cases from the authors' institution are discussed that demonstrate how SSTR PET influenced both diagnosis and treatment strategy.

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.

Medical therapy is typically ineffective or provides only transient relief,2 and stereotactic radiosurgery is often less effective than direct surgical decompression.3 While the retrosigmoid corridor is conventional, the anterior petrosal (Kawase) approach offers unique advantages for tumors involving the petrous apex and Meckel's cave.4-5 Approximately one-third of these tumors cause a concurrent neurovascular conflict.6 CASE DESCRIPTION: A 70-year-old woman, history of breast cancer, presented with Carbamazepine refractory sTN and suicidal ideation secondary to a petrous apex tumor with concurrent SCA compression...The anterior petrosal approach provides short, direct access to pre- and suprameatal pathology while avoiding manipulation of the lower cranial nerves. ESSENTIAL STEPS: frontotemporal craniotomy, MMA coagulation and division, posterior-to-anterior dural peeling to identify GSPN, identifying medial petrous ridge, petrous apex drilling guided by studying the preoperative CT scan, dural opening and dividing the tentorium (avoiding trochlear nerve), tumor resection from the trigeminal branches and AICA, SCA dissection from the trigeminal root entry zone, and Teflon interposition to address the dual-mechanism compression.

Importantly, co-targeting these pathways was able to overcome resistance to TEADi and was superior to MEK/mTOR/FAK inhibition alone. These studies provide a compelling proof-of-concept that TEADi represents a novel therapeutic vulnerability in meningioma and reveal adaptive signaling responses that can be therapeutically exploited.