Brain Cancer

Astrocytoma was the most prevalent pathology in this study. H3K27M mutation did not significantly affect survival in high-grade spinal astrocytoma, while high Ki-67 and p53 expression correlated with poorer prognosis. Tumor length was associated with short-term but not long-term neurological function. Long-term neurological outcomes were mainly linked to inherent tumor properties and postoperative neurological status; postoperative PLR changes may partly indicate long-term neurological function.

Our study provides a non-invasive method to identify glioma phenotypic subtypes, reveal distinct signaling pathways, and define therapeutically homogeneous patient subgroups that could guide targeted therapy.

We have shown that 2p24.3 microduplications that include MYCN predispose to childhood embryonal tumours and should be routinely assessed when WT or neuroblastoma predisposition is suspected. We have also shown that there does not appear to be any increased incidence of childhood tumours when DDX1 alone is duplicated.

Experimental validation using the MTT assay on U87 glioblastoma cells demonstrated that compound 1h exhibited potent cytotoxicity (IC₅₀ = 16.57 ± 0.90μM), significantly outperforming temozolomide. Overall, this study presents the first integrated green-synthetic and computational-experimental evaluation of DHQs against U87 cells, highlighting compound 1h as a promising lead for glioblastoma drug discovery.

P=N/A, N=94, Recruiting, Tata Memorial Centre | Phase classification: P3 --> P=N/A

P=N/A, N=500, Recruiting, Tianjin Medical University

P=N/A, N=55, Enrolling by invitation, Mayo Clinic | Not yet recruiting --> Enrolling by invitation

P2, N=75, Recruiting, BioNTech SE | Not yet recruiting --> Recruiting

P2, N=40, Recruiting, University of Vermont Medical Center | Not yet recruiting --> Recruiting | Trial completion date: Dec 2024 --> Jun 2027 | Trial primary completion date: Jun 2024 --> Dec 2026

P1/2, N=329, Active, not recruiting, Amgen | Recruiting --> Active, not recruiting | N=649 --> 329

Senolytic plus senogenic combinations demonstrate robust preclinical efficacy in reducing tumor growth and senescent burden while promoting apoptosis across diverse in vivo models. These findings highlight senotherapy as a promising adjunct to conventional senescence-inducing anticancer therapies and underscore the need for standardized in vivo methodologies and translational studies to guide clinical application. This review protocol was prospectively registered on PROSPERO (registration number: CRD420251161998).