Glioma

In our patient, the sarcomatous component exhibited p53 and OLIG2 immunohistochemical expression. Molecular analysis revealed IDH and TERT mutations, as well as 1p/19q and CDKN2A deletions.

The SaCas9-KKH induced a genomic deletion, resulting in lowered mmu-miR-21a levels in the brain, leading to reduced tumor growth and improved overall survival. In this study, we demonstrated that disruption of genomic mmu-miR-21a with a single AAV vector influenced glioma development resulting in beneficial anti-tumor outcomes in GB-bearing mice.

Functional validation in patient-derived glioma stem cells and animal models highlights nucleotide metabolism as a promising therapy target for gliomas. This integrated multi-omics analysis introduces a proteomic classification for gliomas and identifies DPYD and TYMP as key metabolic biomarkers, offering insights into glioma pathogenesis and potential treatment strategies.

P=N/A, N=60, Active, not recruiting, Maastricht Radiation Oncology | Trial completion date: Sep 2024 --> Sep 2025 | Trial primary completion date: Sep 2024 --> Sep 2025

P2, N=60, Not yet recruiting, Tata Memorial Centre | Initiation date: Aug 2024 --> Jan 2025

High levels of HIF-1α expression were associated with poorer survival outcomes and other clinicopathological characteristics of glioblastoma. Integrating HIF-1α into prognostic tools for glioblastoma aids in predicting survival, categorising risk, and advising patients on suitable treatment regimens.

In conclusion, our data show that C1GALT1 enhances the progression of glioma by regulated the O-glycosylation and phosphorylation of EGFR and the subsequent downstream AKT/ERK signaling pathway. Therefore, C1GALT1 represents a potential target for the diagnosis and treatment of glioma.

The MiCBO-TF model represents a powerful platform for both mechanistic investigations and the development of precision medicine approaches for DMG.

To lay the groundwork for the future rational optimization of this promising class of compounds, the molecular bases of DM1 and DM2 activity were investigated by modelling their interaction with hCav3.1 channels. The calculated binding modes of DM1 and DM2 to hCav3.1 channels partially mirrored that of the selective Cav3.1 blocker Z944, paving the way for future lead optimization.

Silencing RPS3A inhibited autophagy in U251 cells, whereas rapamycin, an activator of autophagy, reversed the inhibitory effect of RPS3A silencing on TAM M2 polarization...Overexpression of CSF1 promoted the proliferation and invasion of U251 cells and reversed the inhibitory effect of RPS3A silencing on TAM proliferation and invasion, but had no effect on TAM M2 polarization. The results of in vivo experiments showed that knockdown of RPS3A significantly inhibited glioma tumor growth and metastasis in vivo. This study revealed that RPS3A recruited TAMs by upregulating E4F1-mediated transcription activation of CSF1, and promoted the M2 polarization of TAMs through autophagy, promoting glioma cell malignant growth and tumor progression.

Rapid central pathology review and molecular testing for eligibility was feasible. The protocol therapy including radiation, veliparib and temozolomide was well tolerated but failed to improve outcome compared to clinically and molecularly matched historical control cohorts treated with higher doses of alkylator chemotherapy.

In conclusion, pedHGG-RTK2A/B tumors are characterized by highly diffuse-infiltrating growth patterns and specific radiological and histo-molecular features. By comprehensively characterizing methylation-based tumors, the chance to develop specific and effective therapy concepts for these detrimental tumors increases.

CHI3L2 expression may be specific for cancer cells in IDC and involved in cross-talk with the tumor microenvironment. Our study has shown that IDC cancer cells express the CHI3L2 protein, possibly indicating a novel function of this protein.

Notably, flubendazole could damage the glioblastoma stem cells (GSC) that are typically resistant to other therapies, thereby possessing advantages in stopping glioma recurrence. This study delved into the mechanisms of flubendazole-induced ferroptosis in glioma, broadening its application and providing new ideas for new uses of other old drugs.

P1, N=21, Active, not recruiting, University of Florida | Trial completion date: Jun 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jun 2025

P2, N=134, Recruiting, Academic and Community Cancer Research United | Not yet recruiting --> Recruiting

P1, N=59, Active, not recruiting, Children's Oncology Group | Trial completion date: Sep 2024 --> Sep 2025

Our preclinical and clinical data strongly support the further development of PARPis together with DNA damage stress-inducing treatment regimens for DHG-H3G34R_ATRX.

To the best of our knowledge, this study is the first comprehensive analysis of the mechanism of DSN1 leading to poor prognosis of LGG, which provides a new perspective for revealing the pathogenesis of LGG. DSN1 or its methylation has diagnostic value for the prognosis of glioma, and may become a new biological target of anti-tumor immunotherapy.

Furthermore, inhibiting the PI3K/Akt pathway effectively blocked VCAN-mediated glioma progression. These findings provide valuable insights into the mechanisms underlying glioma recurrence and suggest that targeting both VCAN and the PI3K/Akt pathway could represent a promising therapeutic strategy for managing recurrent gliomas.

This study shows that the incorporation of molecular testing can considerably improve brain tumor diagnoses in Nigeria. Furthermore, this study highlights the diagnostic challenges in resource-limited settings and what is at stake in the global disparities of brain tumor diagnosis.

In recent years, it has been shown that dysregulation of molecular mechanisms in many LncRNAs such as MIR22HG, HULC, AGAP2-AS1, MALAT1, PVT1, TTTY14, HOTAIRM1, PTAR, LPP-AS2, LINC00336, and TINCR are connected with the GBM. Therefore, this scientific review paper focused on the molecular mechanisms of these LncRNAs in the context of GBM.

Hydrogel-generated gradients of murine CXCL10, linked to intratumorally injected hydrogel solutions via azidoester linkers, resulted in significant recruitment of CD8+ T-cells and the attenuation of tumor growth in a "cold" syngeneic melanoma model. This study highlights a highly customizable, hydrogel-based delivery system for local protein therapeutic administration to meet diverse clinical needs.

Finally, analysis of immune signatures and clinical characteristics implied that, the activity of the innate immune, diagnostic age, clinical stage, Tumor-Node-Metastasis (TNM) stage and immune types, might play specific roles in modulating tumor prognosis. The study demonstrated that YTH family genes had the potential to predict tumor prognosis, in which the YTHScore illustrated equal ability to predict tumor prognosis compared to RWEScore, thus providing insights into prognostic biomarkers and therapeutic targets at the pan-cancer level.

Treatment of cells with the AKT inhibitors MK2206 and GSK2110183 revealed that the PRKAA1 overexpression group was less sensitive to AKT inhibitors than the negative control group. Taken together, PRKAA1 can be used as a potential prognostic marker and new target for tumor immunotherapy.

By using the novel PDX platform, the results presented in this study demonstrate that the treatments with Palbociclib or Dabrafenib/Trametinib significantly reduced tumor size. In conclusion, PDX models offer a deeper understanding of eGBM at the genomic level and facilitate the identification of potential therapeutic targets. Further translational studies of this novel PDX model hold promise for advancing the diagnosis and treatment of this specific subtype of glioblastoma.

This kind of amplified radiodynamic-ferroptosis therapeutic strategy could remarkably inhibit glioma progression in an orthotopic GBM mouse model. Our study demonstrates the potential of PFeD@Ang for GBM treatment via targeted delivery and combinational therapeutic actions of RDT and ferroptosis therapy.

Our data indicates that DLGAP3 is a potential tumor suppressor and valuable prognostic biomarker in gliomas.

Our findings provided that SLITRK2 may function as a biomarker by regulating immune cell infiltration. In addition, we verified that high SLITRK2 expression was correlated with poor prognosis in GC.

Recent studies emphasize the genetic differences between cerebellar and supratentorial tumours, with new treatments targetting specific molecular abnormalities. Immunotherapy has shown limited effectiveness due to the unique tumour environment in cHGG, and further research is required to improve treatment strategies for these rare tumours.

P2, N=95, Active, not recruiting, Nuvation Bio Inc. | Recruiting --> Active, not recruiting

P=N/A, N=187, Recruiting, Institut du Cancer de Montpellier - Val d'Aurelle | Not yet recruiting --> Recruiting

They have been evaluated both alone and in combination with radiotherapy, temozolomide, anti-angiogenic agents, immunotherapy and other new drugs in newly diagnosed or recurrent glioma...In conclusion, early phase studies have shown promising anti-tumour activity of PARPi that should be confirmed in larger prospective and randomised trials. In addition, the development of novel PARPi with improved blood brain barrier (BBB) penetration and PARP inhibitor activity with new synergistic treatment combinations seems promising and needs to be further explored.

In a clinically relevant resection and recurrence model of patient-derived human GBM, we demonstrate that nanoengineered MSCs are not "donor agnostic" and efficacy is influenced by the inherent suitability of the MSC to the cargo. Therefore, donor profiles hold greater influence in determining downstream outcomes than the technical capabilities of the engineering technology.

Elevated serum IL-10 and GFPA levels in patients with brain glioma are associated with postoperative brain injury. IL-10 and GFPA can serve as valuable indicators for the prognostic evaluation of patients with brain gliomas.

Future research should focus on integrating diverse data types, including advanced imaging, semantics and clinical data while also aiming to standardise the collection and integration of multimodal data. This approach will enhance clinical applicability and consistency.

ARV-825 may play a role in modulating drug resistance by degrading the BRD4 protein, thereby exerting anti-glioma effects. Furthermore, mechanistic exploration revealed that T+A@Glu-NPs degraded the BRD4 protein, leading to the downregulation of Notch1 gene transcription and the inhibition of the Notch1 signaling pathway, thereby augmenting the therapeutic efficacy of glioma chemotherapy. Taken together, the findings suggest that T+A@Glu-NPs represents a novel and promising therapeutic strategy for glioma chemotherapy.

CNN-based classifiers achieved an AUROC of 86.1, 95% CI (85.0, 87.3), while the tumour-location-guided CNNs outperformed the other classifiers with an average AUROC of 88.64, 95% CI (87.6, 89.7), which was statistically significant (P-value .0018). Incorporating tumour location probability maps into CNN models led to significant improvements for molecular subtype identification of pLGG.

4 pts received TT at recurrence, within clinical trials: one with grade 3 meningioma and ALK rearrangement treated with alectinib, one with PTCH1 mutant medulloblastoma treated with vismodegib, and two with high TMB treated with nivolumab/ipilumumab. The incidence of targettable molecular alterations in adult CNS tumor patients was lower than in GBM. Nevertheless, in a few selected cases TT have the potential to increase treatment options at recurrence and improve outcomes.

The findings suggest that symptomatic glioma enhances inflammatory responses linked to poor prognosis and chemoresistance. This supports the hypothesis that immediate treatment of incidental glioma may improve patient outcomes over a wait-and-see approach.

In the early postoperative period, two patients had motor aphasia and hemiparesis, which further regressed. The results of a small group of patients allow to consider sPDT with 5-ALA as a promising technique to treat patients with recurrent high-grade gliomas in functionally relevant brain areas and require further prospective assessment.

In cell-based studies, ALK2 inhibitors effectively attenuated activin A and BMP-induced Phosphorylated SMAD1/5 activation in fibroblasts from individuals with FOP in a dose-dependent manner. Thus, CDD-2789 is a valuable tool compound for further investigation of the biological functions of ALK2 and ALK1 and the therapeutic potential of specific inhibition of ALK2.