Mesothelioma

According to the pharmacogenomic analysis from GDSC2 dataset, tumor cells that express higher DNA2 are more sensitive to Tozasertib, and Daporinad. DNA2 is at the core of several interrelated modules, including flap processing, telomerase extension, and cell-cycle progression, according to the enrichment study. These findings have suggested DNA2 as a therapeutic vulnerability in cancer, a context-dependent biomarker with implications for treatment response, prognosis, and immunity.

Furthermore, these cells produced anti-tumor effects in a novel 3D tumor spheroid model system established to evaluate the potency of reactive cells against tumors including pancreatic, cervical, and colorectal cancer and mesothelioma. These preclinical findings lay the groundwork for further exploration of MSLN as a potential immunotherapeutic target for T cells via the native T cell receptor.

Trop-2 was expressed in 20% of PMs, exclusively in epithelioid histology, associated with advanced disease and poor survival outcomes. These results support the prospective evaluation of Trop-2-targeted therapies in PM.

Importantly, these cells display a favorable safety profile, with minimal evidence of graft-versus-host disease, cytokine release syndrome, brain infiltration or neurotoxicity, and no detectable off-tumor effects. Collectively, these findings support the development of a clinically translatable, off-the-shelf CAR-NKT cell therapy for the treatment of MPM.

In sporadic meningiomas, BAP1 alterations are rare but define an aggressive molecular subset with poor outcomes. Here, we describe a patient with BAP1-TPDS and multifocal cranial meningiomas who experienced exceptional radiographic regression of her tumors while receiving dual immune checkpoint blockade for metastatic uveal melanoma.

One case harbored an ALK rearrangement, guiding effective targeted therapy with alectinib...Accurate histopathological assessment is essential to establish a correct diagnosis and guide appropriate therapy. A multidisciplinary approach remains the cornerstone of diagnostic precision in CUP cases.

Finally, this cascade triggers immunogenic cell death and orchestrates a chemokine storm, which is hypothesized to facilitate the conversion of the tumor microenvironment from an immune "cold" to a "hot" phenotype. Collectively, by integrating the physical disintegration of subcellular structures with immunological remodeling, TTFields may offer a hypothetical theoretical framework for overcoming therapeutic resistance in MPM.

P1, N=74, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

P3, N=861, Active, not recruiting, AstraZeneca | Recruiting --> Active, not recruiting | Trial primary completion date: Nov 2027 --> Nov 2028

P2, N=31, Completed, Biotheus Inc. | Recruiting --> Completed | N=55 --> 31 | Trial completion date: Jun 2026 --> Mar 2026 | Trial primary completion date: Jun 2026 --> Mar 2026

For nearly twenty years, platinum-pemetrexed chemotherapy has persisted as the unchanged standard treatment; although recent progress in immunotherapy has modestly disrupted this therapeutic plateau, survival outcomes remain disappointingly limited...Preclinical and early clinical data demonstrate that EZH2 inhibitors-including tazemetostat, valemetostat, GSK126, EPZ011989, tulmimetostat, and novel PROTAC-based degraders such as MS1943-can suppress tumor progression, modulate the tumor immune microenvironment, and restore therapeutic sensitivity...Further understanding the dual canonical and non-canonical roles of EZH2 in tumor biology will be key to optimizing targeted and combinatorial treatment strategies. Future research should focus on translating EZH2 inhibition into clinical benefit, identifying predictive biomarkers of response, and exploring rational combinations with chemotherapy, targeted drugs, or immunotherapy to improve survival outcomes in mesothelioma patients.

PTPA promotes oncogene-induced senescence (OIS) in MPM. By preventing OIS, heterozygous PTPA loss may contribute to mesothelial transformation and carboplatin resistance.