Glioblastoma

P4, N=175, Recruiting, Orszagos Onkologiai Intezet | Not yet recruiting --> Recruiting

Furthermore, static magnetic fields have been reported to increase apoptosis, inhibit proliferation, and may offer a complementary treatment with low toxicity. These findings suggest that magnetic-field-based approaches offer an innovative strategy for GBM treatment.

Integration with TCGA data identified 10 oncogenic genes (PARP10, OAS1, OAS3, PRR4, ZNFX1, HELZ2, SP110, CSRNP1, DDX3L, and PARP14) dysregulated across 20+ cancer types; qPCR confirmed their consistent downregulation posttreatment in both cell lines (P<0.05). This study establishes parimifasor's antitumor efficacy via the suppression of immune pathway-associated oncogenes, supporting its repurposing as a cancer therapeutic agent and providing biomarker candidates for clinical development.

Drug sensitivity analysis revealed differential half-maximal inhibitory concentration (IC50) values for 20 anticancer agents between risk groups. Our findings suggest that SOX21-AS1 may influence the tumor microenvironment through the modulation of the immune checkpoint CD274, potentially serving as a novel prognostic indicator and a target for immunotherapeutic strategies in GBM.

Moreover, this thorough analysis can facilitate the exploration of potential disease-causing SNPs in the TFEB gene and assist in identifying effective drugs or pharmacological targets. Consequently, further experimental mutational research, genome-wide association studies, and clinical-based studies are essential to validate these findings.

In parallel, TRIM28 interacted with MCM7 and promoted its K63-dependent ubiquitination. These findings reveal a TRIM28-MCM7 axis that supports DNA replication-associated proliferation through transcriptional activation and K63-dependent post-translational regulation.

P-TNTs, which are tightly associated in situ with endothelial-pericyte combined sprouts, appear to play a dual role during vessel collateralization by bridging the gap between distant vessels and guiding vascular outgrowth. The complementary cellular distribution of c-KIT and SCF observed in endothelial cells and pericytes suggests that both endothelial autocrine/paracrine SCF/c-KIT signaling and pericyte-derived paracrine/juxtacrine SCF cues may contribute to the pericyte-driven mode of vessel branching. Similar observations in GB samples further suggest a potential involvement of pericytes and their P-TNTs in tumor vascularization, although sprouting endothelial cells displayed distinct subcellular patterns of c-KIT expression in fetal versus GB tissues.

Emerging applications in other cancer types are also summarized and discussed. Throughout the review the focus is more on a critical discussion of concepts and relevant publications and their merits and shortcomings than trying to achieve complete coverage of the voluminous literature.

Through structure-based virtual screening, our results suggest that Ziprasidone and Apomorphine may disrupt the BARD1-XRCC5 interaction...Our findings unveil a novel LLPS-mediated mechanism by which BARD1 confers TMZ resistance in GBM, positioning it as a prognostic marker and a therapeutic target. Targeting the BARD1-XRCC5 axis presents a promising strategy to overcome chemoresistance.

In conclusion, this study identifies a previously uncharacterized HIF-1α/circSPECC1/IGF2BP2/PGK1 axis that drives metabolic adaptation and TMZ resistance in GBM. Targeting this axis overcomes acquired chemoresistance, positioning circSPECC1 as both a prognostic biomarker and a therapeutic vulnerability in hypoxic GBM niches.

Histopathological analysis showed that the combination group had less cell proliferation (as evidenced by reduced Ki-67 expression) and greater tumor necrosis. This study reveals the synergistic effects of Oncomed and ATO, suggesting a potential combinatorial strategy to address the limitations of current cancer treatments and improve patient outcomes.

Finally, we propose a translational framework that integrates standardized detection, localization-aware pathology, multi-omics profiling, organoid and patient-derived xenograft validation, AI-assisted inhibitor discovery, RNA-based delivery, and rational combination therapy. Although no TIPE3-targeted therapies have yet reached clinical application, emerging mechanistic and drug discovery studies underscore TIPE3's potential as a valuable biomarker and therapeutic target in precision oncology.