Recent studies have highlighted the complex interplay between immunotherapy and the immune microenvironment in neuro-oncology. One significant finding is the role of the serotonin transporter (SERT) in inhibiting antitumor immunity. Research indicates that SERT is induced in tumor-infiltrating CD8 T cells, and its inhibition using selective serotonin reuptake inhibitors (SSRIs) can significantly suppress tumor growth while enhancing T cell antitumor immunity in various mouse models (ref: Li doi.org/10.1016/j.cell.2025.04.032/). Additionally, the cognitive impacts of CAR T cell therapy have been explored, revealing that such therapies can impair cognitive function and induce persistent CNS immune responses, characterized by microglial reactivity and elevated cytokines, which disrupt neurogenesis (ref: Geraghty doi.org/10.1016/j.cell.2025.03.041/). Furthermore, glioblastoma has been shown to remodel neuronal circuits, leading to regional immunosuppression, which is marked by distinct immune cell compositions and the enrichment of anti-inflammatory tumor-associated macrophages (TAMs) (ref: Nejo doi.org/10.1038/s41467-025-60074-z/). These findings collectively underscore the need for a deeper understanding of the immune landscape in neuro-oncology to improve therapeutic strategies.

The exploration of molecular and genetic mechanisms in glioma has yielded significant insights into tumor biology and potential therapeutic targets. A comprehensive genomic analysis of diffuse gliomas revealed a complex landscape of recurrent mutations and structural variants, providing a high-resolution map that could inform future studies (ref: Kinnersley doi.org/10.1038/s41467-025-59156-9/). Additionally, the identification of dipeptidase-1 as a novel vascular marker in hypermetabolic glioblastoma lesions highlights the intricate relationship between metabolic states and genomic evolution within tumors (ref: Anand doi.org/10.1093/neuonc/). Furthermore, the development of a tissue-specific atlas of protein-protein associations has enabled the prioritization of candidate disease genes, enhancing our understanding of glioma pathogenesis (ref: Laman Trip doi.org/10.1038/s41587-025-02659-z/). These studies collectively emphasize the importance of integrating molecular profiling with therapeutic strategies to address the challenges posed by gliomas.

Research into the tumor microenvironment and metabolism has revealed critical insights into glioblastoma (GBM) and melanoma treatment strategies. A multicentric observational study demonstrated the feasibility of multiomics tumor profiling in melanoma, utilizing nine independent technologies to analyze patient samples and generate extensive data for precision oncology (ref: Miglino doi.org/10.1038/s41591-025-03715-6/). In GBM, the upregulation of bromodomain-containing protein 4 (BRD4) has been identified as a key factor contributing to temozolomide resistance, suggesting that targeting this pathway could enhance treatment efficacy (ref: Xu doi.org/10.1002/adma.202504253/). Moreover, the discovery of polyamine acetylation's role in mediating metabolic crosstalk between cancer cells and myeloid cells highlights the metabolic reprogramming that characterizes GBM and its influence on tumor-immune interactions (ref: Rana doi.org/10.1093/neuonc/). These findings underscore the necessity of understanding metabolic pathways within the tumor microenvironment to develop effective therapeutic interventions.

Clinical outcomes and treatment strategies in neuro-oncology have been significantly influenced by recent advancements in understanding tumor biology and patient management. A case study highlighted the successful pregnancy outcome of a patient with ALK-positive non-small cell lung cancer (NSCLC) treated with lorlatinib, demonstrating the importance of maternal-fetal pharmacokinetics in managing cancer during pregnancy (ref: Yao doi.org/10.1016/j.jtho.2025.05.017/). Additionally, the impact of corticosteroid administration on glioblastoma imaging has been examined, revealing that corticosteroids can artificially reduce contrast-enhancing tumor volume, complicating treatment assessments (ref: Sanvito doi.org/10.1093/neuonc/). Furthermore, the reannotation of cancer mutations based on expressed RNA transcripts has uncovered functional non-coding mutations in melanoma, emphasizing the need for accurate mutation characterization in treatment planning (ref: Pepe doi.org/10.1016/j.ajhg.2025.04.005/). These studies collectively highlight the evolving landscape of clinical strategies in neuro-oncology, emphasizing the integration of molecular insights into patient care.

The neurodevelopmental aspects of brain tumors have garnered attention, particularly regarding the long-term effects of cancer therapies on cognitive function. Research has shown that CAR T cell therapy can lead to cognitive impairments in mouse models, highlighting the need to consider the neurotoxic effects of immunotherapies in both pediatric and adult populations (ref: Geraghty doi.org/10.1016/j.cell.2025.03.041/). Additionally, a comprehensive analysis of pediatric high-grade gliomas (pHGGs) revealed significant differences in the immune microenvironment compared to adult gliomas, which may contribute to the limited efficacy of current treatment strategies (ref: LaBelle doi.org/10.1016/j.xcrm.2025.102095/). Furthermore, the investigation of hypermetabolic lesions in glioblastoma has provided insights into the spatial genomic evolution of tumors, emphasizing the importance of understanding these dynamics for developing effective therapeutic strategies (ref: Anand doi.org/10.1093/neuonc/). These findings underscore the critical need to address the neurodevelopmental implications of brain tumors and their treatments.

Innovations in tumor profiling and therapeutics are reshaping the landscape of cancer treatment, particularly in neuro-oncology. The feasibility of multiomics profiling has been demonstrated in melanoma, where extensive data generation from patient samples has the potential to guide personalized treatment decisions (ref: Miglino doi.org/10.1038/s41591-025-03715-6/). Additionally, the shift from bulk to infiltrative growth in glioblastoma has been linked to microglia alignment, suggesting that understanding tumor-associated immune cell interactions is crucial for developing effective therapies (ref: Kang doi.org/10.1038/s43018-025-00985-4/). Moreover, the reannotation of cancer mutations has revealed functional non-coding mutations that may influence therapeutic outcomes, highlighting the importance of accurate genomic characterization in treatment planning (ref: Pepe doi.org/10.1016/j.ajhg.2025.04.005/). These advancements emphasize the need for integrating innovative profiling techniques with therapeutic strategies to enhance patient outcomes in neuro-oncology.

Pediatric neuro-oncology has seen significant advancements in understanding the unique challenges posed by childhood brain tumors. Research on CAR T cell therapy has revealed potential cognitive impairments associated with treatment, underscoring the need for careful monitoring of neurodevelopmental outcomes in young patients (ref: Geraghty doi.org/10.1016/j.cell.2025.03.041/). Furthermore, the exploration of glioblastoma metabolic lesions has provided insights into the genomic evolution of tumors, emphasizing the importance of understanding these dynamics for developing effective therapeutic strategies (ref: Anand doi.org/10.1093/neuonc/). Additionally, the creation of a tissue-specific atlas of protein-protein associations has facilitated the prioritization of candidate disease genes, enhancing our understanding of pediatric brain tumor biology (ref: Laman Trip doi.org/10.1038/s41587-025-02659-z/). These findings highlight the critical need for tailored approaches in pediatric neuro-oncology to address the unique biological and therapeutic challenges faced by this population.