GRIN2A (Glutamate Ionotropic Receptor NMDA Type Subunit 2A)

This study was designed to systematically investigate the prognostic significance of palmitoylation-related genes in GBM. GABRB2, NCF2, and GRIN2A are expected to become new biomarkers for GBM.

P3, N=40, Recruiting, Meyer Children's Hospital IRCCS

Perturbagen analysis nominated signature-reversing compounds across sexes, including histone deacetylase inhibitors, Aurora kinase inhibitors, microtubule-targeting agents such as vindesine, and multi-kinase inhibitors targeting VEGFR, PDGFR, FLT3, PI3K, and MTOR. Glioma grade comparisons reveal a shared neuronal-synaptic program accompanied by sex-specific transcriptional remodeling. These findings support sex-aware therapeutic strategies that pair modulation of neuron-glioma coupling with chromatin- or receptor tyrosine kinase/angiogenic-targeted agents, and they nominate biomarkers such as GLI1, MYOD1, GCGR, PRLHR, and HIST1H2BH for near-term validation.

Non-neuronal cell types including astrocytes, oligodendrocytes, and vascular cells also exhibited region-specific translational changes in neurotransmitter transport, lipid synthesis, myelination, and stress response pathways, some of which co-varied with regional neuron state. Together, our study reveals brain-wide translation dysregulation as a critical mechanism underlying SCZ pathophysiology.

Our results provide novel molecular insights regarding the roles of non-CNS cancer pathology and treatments in the brain related to calcium signaling and pro-survival/plasticity-related pathways. Our findings also point to potential treatments for cognitive effects of cancer.

Our findings demonstrate AD-specific increases in ES-GluN2B expression and a significant downregulation in PSA-NCAM levels, distinguishing AD from normal aging, potentially driven by Aβ-induced downregulation of biosynthetic enzymes ST8Sia4 and UDP-E. This underscores a potential link between PSA-NCAM expression and Aβ activity in AD, as well as possible therapeutic targets for AD intervention.

Functional studies revealed that inhibition of the mutated oncogene ROS1 using crizotinib induces death in infected leukocytes, confirming its role in transformation...Our findings provide new insights into how T. annulata reprograms host cells through genomic instability and mutations, identifying ROS1 and TP53 as critical targets for therapeutic intervention. This work advances understanding of parasite-induced oncogenic transformation and offers pathways for future research.

The peptide group molecules, Phospholipase A2, Klotho protein, and soluble urokinase plasminogen activator receptor (suPAR), also remain consistently important. From the perspective of SZ as a disease associated with neuronal damage, biomarkers correlating with brain injury, neuron-specific enolase (NSE), and S100B protein should be considered.

The melanomas found in these veterans showed a significantly higher frequency of variants in CDKN2A/B; a significantly lower frequency of variants in ROS1, GRIN2A, KDR, KMT2C (MLL3), KMT2D (MLL2), LRP1B, PTPRT, PTCH1, FAT4, and PREX2; and a significantly higher frequency of tumor mutational burdens exceeding 10 mutations/megabase. The presence of statistically significant differences between the genomic findings from the veterans' melanomas and those of general population melanomas from reference databases suggests that additional research is warranted to corroborate these differences and clarify their etiologic, prognostic, and therapeutic relevance.

Additionally, Aβ suppressed PSA-NCAM biosynthetic enzymes ST8Sia4 and UDP-E linking Aβ to impaired polysialylation. These findings highlight distinct regulatory patterns of ES-GluN2B and PSA-NCAM in AD versus normal aging and support a model in which impaired PSA-NCAM buffering facilitates pathological ES-GluN2B signaling and plasticity loss in AD progression.

This OSRG-based model demonstrates strong prognostic potential, stratifying CCA patients by risk and survival outcomes. The model provides insights into personalized treatment strategies, potentially advancing therapeutic interventions for CCA.

Genomic profiling improves precision management of CRLM, facilitating tailored conversion strategies and better prognostic prediction. Future studies should validate these findings in prospective cohorts to refine personalized treatment for patients with initially unresectable CRLM.