The clinical, neuroradiological and surgical definition of hypothalamic involvement is a fundamental factor related to poor postoperative outcome, progressive obesity and neuropsychological impairment in children after surgical removal of craniopharyngiomaThe previously assumed 'gold-standard' objective of a primary radical removal of the lesion in all cases needs to be replaced with the new paradigm of a limited resection plus focused radiotherapy in patients with craniopharyngioma and hypothalamic lesions

Glioblastoma (GBM) is the most common high-grade primary malignant brain tumor, characterized by a notably poor prognosis. Current treatments for GBM have shown limited effectiveness in improving patient survival, highlighting the urgent need for effective therapeutic strategies. Combination therapy offers significant potential in overcoming resistance by targeting multiple signaling pathways; however, it often comes with increased toxicity compared to monotherapy. Co-encapsulating multiple therapeutic agents into a tumor-targeted drug delivery platform holds promise for overcoming these limitations and improving treatment outcomes.

In an unprecedented advancement in glioblastoma treatment, a groundbreaking phase I/II clinical trial known as GLORIA has unveiled promising results combining L-RNA aptamer-based CXCL12 inhibition with radiotherapy and bevacizumab in newly diagnosed patients. This innovative therapeutic approach targets the molecular microenvironment of glioblastoma, offering renewed hope in a field long hindered by the aggressive nature and poor prognosis of this brain malignancy. The recently expanded trial, detailed in a 2026 publication in Nature Communications by Giordano et al., marks a significant milestone in neuro-oncology, especially by leveraging molecular precision to overcome resistance mechanisms intrinsic to glioblastoma.

In a groundbreaking study set to reshape our understanding of glioblastoma progression, researchers have identified glutamate decarboxylase 1 (GAD1) as a critical suppressor of this aggressive brain tumor through modulation of the GSK3β/β-catenin signaling pathway. Glioblastoma, notorious for its rapid growth and poor prognosis, remains one of the most challenging malignancies to treat effectively. This discovery opens new avenues for therapeutic intervention targeting the molecular underpinnings driving tumor proliferation and invasiveness.

[64Cu]Cu-αCD11b Db is a high-affinity and stable diabody, which can quantify CD11b-positive TAMCs in the tumor microenvironment, particularly when the molar activity of the administered [64Cu]Cu-αCD11b Db is optimized for managing the CD11b antigen sink in the spleen, liver, and bone marrow.

Macrophage-mediated phagocytosis of tumor cells elicits potent antitumor immunity. Nonetheless, sole-blockade of the anti-phagocytosis molecule CD47 has yielded insufficient therapeutic outcomes. Here, we report that glioblastoma (GBM) cells expressed abundant levels of phagocytosis checkpoint CD24. We further show that dual blockade of CD24 and CD47 synergistically enhances the pro-phagocytic activity of macrophages, thereby improving tumor antigen cross-presentation and activating the cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS-STING) pathway. This innate immune activation facilitates T cell infiltration into tumors and sensitizes tumors to anti-PD1 therapy, improving survival outcomes in murine GBM models, including immunosuppressive tumors reflecting human GBM-like features. Thus, our results indicate that dual-phagocytosis checkpoint blockade offers a promising therapeutic avenue to potentiate cancer immunotherapy.

Survival of patients with glioblastoma (GB) treated with standard of care (SOC) surgery, radiotherapy, and temozolomide is 15 months with progression free survival at 6 months (PFS-6 M) of 53.9%. In vivo studies showed increased survival in mice with GB treated with niacin. This is a first in human Phase I-II study aiming to evaluate safety and efficacy of controlled-release niacin (NiacinCRT ™) added to SOC.

Valle said she had no side effects from participating in the trial. Four years after her diagnosis with glioblastoma, she has no evidence of disease. It's a rare positive outcome for a disease that kills most patients within 18 months.  "I am truly an outlier," Valle, now 41, said. 

Our work introduces for the first time the use of novel bioinspired membranes designed as a potential patch platform for localized intervention in glioblastoma after surgery, representing a promising advancement in this field. Despite the rapid growth in mussel-inspired research, this work is distinctly innovative. Unlike the common hydrogel and coatings focus, our solid, free-standing bioadhesive membranes could offer a unique solution for glioblastoma treatment. Moreover, their selective toxicity against cancer cells, while sparing healthy astrocytes in vitro, highlights their potential for a novel and targeted application. Our bioinspired membrane addresses critical challenges such as adhesion in humid environments, infection prevention, and biocompatibility. The adhesive properties of the membrane ensure it stays in place, allowing for the sustained delivery of the localized cytotoxic effect to the affected area. This novel approach offers a localized and sustained therapeutic concept based on ROS modulation, that could complement the current glioblastoma treatment paradigm.

When glioblastoma tumors are treated with chemotherapy, levels of miR-181d drop. This drop amplifies the differences among individual cells within the tumor, thereby allowing more cells to make more MGMT and survive treatment. The research team found that administering miR-181d into the tumor can reduce this effect, making the cancer cells behave more uniformly, and importantly, more likely to respond to chemotherapy.

High-grade glioma is one of the deadliest primary tumors of the central nervous system. Despite the many novel immunotherapies currently in development, it has been difficult to achieve breakthrough results in clinical studies. The reason may be due to the suppressive tumor microenvironment of gliomas that limits the function of specific immune cells (e.g., T cells) which are currently the primary targets of immunotherapy. However, tumor-associated macrophage, which are enriched in tumors, plays an important role in the development of GBM and is becoming a research hotspot for immunotherapy. This review focuses on current research advances in the use of macrophages as therapeutic targets or therapeutic tools for gliomas, and provides some potential research directions.

Ongoing research is trying to change that. A team of scientists from McMaster University and the Hospital for Sick Children (SickKids) in Canada has now identified an inconspicuous type of brain cell that reprograms its communication to support glioblastoma growth. When knocked out in experiments, cancer growth slowed down.Not only did they discover a critical role for a brain cell type previously thought to be harmless in cancer development, but they also matched it with a drug already on the market. According to the study published in Neuron, the approved HIV medicine Maraviroc extended the lifespan of mice with glioblastoma, demonstrating that the researchers uncovered a potential target to treat a devastating disease.

This systematic review and meta-analysis examines prognostic factors affecting survival after re-resection for recurrent glioblastoma, synthesizing data from 30 studies (1,741 pooled patients). Key findings identify gross total resection and MGMT promoter methylation as strong positive predictors, while age and low preoperative KPS associate with poorer outcomes; adjuvant therapies and time to re-resection showed inconsistent effects.

Bevacizumab (BEV) is known to improve progression-free survival (PFS) but not overall survival (OS) for newly diagnosed glioblastoma (ndGBM). Here, we evaluated the survival outcomes between temozolomide (TMZ)-only and TMZ + BEV treatments stratified based on the cyclooxygenase-2 (COX-2) expression, a rate-limiting enzyme involved in the cancer development.

Despite the limitations of this study, these findings enable evidence-based decision making regarding the use of BEV for the treatment of newly diagnosed GBM. Our study confirms the previous literature concluding that BEV therapy is associated with a prolonged PFS in adult patients diagnosed with newly diagnosed GBM, but has an inconsistent effect on OS. Future research is necessary to define a patient population for whom BEV therapy at diagnosis is indicated.

Glioblastoma (GBM) is a devastating disease with limited treatment options. We find that EdU in combination with the currently used anticancer drug TMZ produces highly significant survival benefits and synergistic effects in preclinical GBM models. This striking effect presumably results from simultaneously engaging distinct DNA repair pathways and offers a potential tool against this disease.

Management of hypothalamic syndrome remains highly challenging. Recently, a risk-adapted, personalized treatment algorithm has been proposed to guide clinical care. Therapeutic interventions such as dextroamphetamine and other centrally acting stimulants, along with glucagon-like peptide-1 receptor (GLP-1R) agonists, and setmelanotide have shown potential in promoting weight reduction. Bariatric surgery has also demonstrated efficacy; however, the use of irreversible surgical techniques in pediatric populations remains ethically and legally contentious. This report summarizes perspectives of future research and clinical progress in diagnostics, treatment, and follow-up of patients with craniopharyngioma.

Des chercheurs ont développé une thérapie CAR-T à base de cellules tueuses naturelles (« natural killer », NK), qui s’est montrée plus efficace que les immunothérapies actuelles contre le cancer du sein triple négatif à un stade avancé – la forme la plus agressive de cancer du sein. La thérapie peut être produite en masse à partir de dons de cellules souches sanguines, ce qui réduirait considérablement son coût de développement. Sa polyvalence permettrait aussi de l’utiliser contre d’autres types de tumeurs solides.

Glioblastoma is unusually resistant to attack by T cells, rendering immune checkpoint inhibitors ineffective. The culprit is a different immune cell, macrophages, which have been recruited to tumors, where they support tumor growth while suppressing the ability of T cells to infiltrate and attack tumors. A team of researchers led by Forest White at the MIT Koch Institute for Integrative Cancer Research used sophisticated immune profiling tools to map out how macrophages evolve from a first-line defense against cancer and other pathogens into a shield that protects the glioblastoma tumor—as well as how the tumor cells themselves are transformed by the encounter.

To overcome the barriers, researchers modified an HSV-1 virus to recognize markers found only on glioblastoma cells. They engineered the virus to express five different immunomodulatory molecules to help reprogram the tumor environment, including IL-12, anti-PD1, a bispecific T cell engager, 15-hydroxyprostaglandin dehydrogenase and anti-TREM2.Researchers also added safety mutations, or "off-switches," that prevent the virus from spreading to neurons or healthy central nervous system cells. So that the reach of the virus could be visualized on PET scan, the team inserted a gene that expresses a protein capable of trapping a PET-tracer molecule.