Glioblastoma represents the most common and lethal form of primary brain cancer, characterized by rapid growth and an intricate ability to evade immune system attacks. A critical barrier to effective treatment has been the tumor’s complex interaction with the immune microenvironment, particularly its manipulation of macrophages—immune cells fundamentally tasked with defending the body against pathogens. Glioblastoma cunningly reprograms these macrophages within its milieu, transforming them into accomplices that support tumor survival, promote growth, and suppress anti-tumor immune responses, thereby creating a protective niche against therapeutic intervention.

Central to this innovative therapeutic design is the identification of Glycoprotein non-metastatic melanoma protein B (GPNMB), a protein abundantly expressed both on glioblastoma cancer cells and the tumor-supportive macrophages. The dual presence of GPNMB in both malignant and immune-supportive cells presented researchers with a unique target: engineering a treatment capable of neutralizing the tumor itself while simultaneously dismantling its immunological sanctuary. This multifaceted approach represents a paradigm shift from traditional therapies that focus solely on eradicating cancer cells without addressing the enabling immune microenvironment.

Leveraging the revolutionary modality of Chimeric Antigen Receptor T-cell therapy (CAR-T), the McMaster team engineered immune effector cells to recognize and bind to GPNMB. CAR-T therapy, which has demonstrated remarkable efficacy in certain hematologic malignancies, involves genetically modifying patient-derived T cells to express receptors that specifically target tumor-associated antigens. In this application, CAR-T cells were tailored to identify GPNMB-expressing cells, enabling a concurrent assault on the cancerous tumor cells and the supportive macrophage population that fosters tumor growth and immune evasion.

Dr. Sheila Singh, senior author and professor of surgery at McMaster, emphasizes the conceptual evolution underlying this research. “Treating glioblastoma requires viewing it not merely as a conglomerate of malignant cells but as a complex ecosystem,” she explains. “Our strategy disrupts this ecosystem by simultaneously taking down both the tumor components and the immune cells that protect and nurture it. This dual-action approach moves us toward eradicating both tumor and its immunosuppressive shield.”

Preclinical investigations encompassing multiple models of glioblastoma, including those directly derived from human patient tumors, have yielded compelling results. These models demonstrated complete elimination of detectable tumors following CAR-T therapy targeting GPNMB and subsequent sustained remission, highlighting the durability of the antitumor response elicited by this approach. Such promising preclinical outcomes strongly suggest the potential for clinical translation, with the goal of overcoming glioblastoma’s notorious treatment resistance and improving patient survival.

This research builds upon prior efforts that explored GPNMB as an immunotherapeutic target across various cancer types. Notably, an initial human clinical trial at the University of Calgary employed GPNMB-specific CAR-T therapy to treat metastatic sarcoma—a cancer originating in connective tissues—with encouraging findings recently published in Nature Cancer. Such cross-cancer applicability underscores GPNMB’s promise as a broadly relevant target and affirms the translational potential of therapies aimed at this molecule.

Despite significant progress, several challenges remain before this innovative therapy can be introduced into clinical practice for glioblastoma patients. The central nervous system’s unique environment, potential off-target effects, and the need for long-term safety evaluation necessitate further rigorous investigation. Dr. Shan Grewal, co-lead author and MD/PhD candidate at McMaster, underscores the intricacy: “While CAR-T therapies have revolutionized treatment for certain blood cancers, their application to brain tumors has faced hurdles. Our findings indicate that targeting both the tumor and the immune system components that sustain it might be the key to unlocking efficacy in such complex solid tumors.”

This study exemplifies a concerted collaborative effort, uniting researchers from prestigious institutions including King’s College London, Northwestern University, the University of Calgary, the University of Toronto, and The Hospital for Sick Children. This multidisciplinary partnership fuses expertise in oncology, immunology, neurosurgery, and molecular biology, fostering comprehensive investigation into this ambitious therapeutic concept.

The researchers acknowledge funding support from numerous prominent organizations devoted to cancer and brain research, including the Terry Fox Research Institute, Brain Canada, the Cancer Research Society, Brain Cancer Canada, and the Brain Tumour Foundation of Canada. Such financial backing underscored the importance and societal urgency of advancing treatment options for devastating brain cancers.

This innovative CAR-T approach, which simultaneously disrupts glioblastoma tumors and their immunosuppressive microenvironment, signifies a hopeful stride forward in neuro-oncology. By addressing the tumor-immune ecosystem as an integrated therapeutic target, this research charts a promising course toward more effective and durable treatments for glioblastoma, setting the stage for forthcoming clinical trials and ultimately, improved patient outcomes in a cancer type that has long defied cure.

Subject of Research: Glioblastoma immunotherapy targeting tumor and tumor-associated macrophages via GPNMB-specific CAR-T cells.

Article Title: (Not provided in the source content)

News Publication Date: 1-Jul-2026

Keywords: glioblastoma, cancer immunotherapy, CAR-T therapy, GPNMB, tumor-associated macrophages, brain cancer, tumor microenvironment, glioma, immuno-oncology, McMaster University, tumor-immune ecosystem

Glioblastoma represents the most common malignant primary brain tumor in adults and is characterized by rapid progression and widespread infiltration. Despite aggressive treatment modalities, including surgery, radiation, and chemotherapy, recurrence is almost inevitable, with median survival after relapse rarely exceeding a year. Traditional systemic therapies often falter against GBM because the blood-brain barrier limits drug and immune cell access, while the tumor microenvironment is adept at subverting immune responses through a range of immunosuppressive mechanisms.

The novel CAR T cell therapy explored by Penn researchers targets two distinct antigens on GBM tumor cells, aiming to enhance tumor recognition and eradication capabilities. Unlike conventional CAR T approaches used in hematological malignancies, this therapy is infused via intracerebroventricular (ICV) injection straight into the CSF bathing the brain. This delivery bypasses the restrictive blood-brain barrier, allowing direct contact with tumor sites and enabling unprecedented real-time monitoring of immune responses through sequential CSF sampling.

Employing advanced single-cell RNA sequencing, the research team meticulously analyzed CSF immune cell populations before treatment and at intervals post-infusion—specifically at days seven and twenty-one. This granular cellular profiling revealed a consistent reshaping of the immune environment triggered by CAR T cell administration, though the quality and nature of this remodeling varied distinctly between patients who responded favorably and those who did not.

Responders demonstrated marked activation of NK cells, a class of innate lymphocytes with potent cytotoxic functions capable of swiftly targeting and killing abnormal or stressed cells, including tumor cells. This NK cell activation correlated with greater tumor shrinkage and extended overall survival, underscoring the critical role of harnessing innate immunity alongside adaptive CAR T cell targeting in combating GBM. The data suggest that an orchestrated interplay between engineered CAR T cells and the endogenous immune compartment amplifies antitumor effects.

Conversely, non-responders exhibited increased proportions of activated Tregs and immunosuppressive myeloid lineage cells within their CSF. These cells contribute to immune tolerance by dampening effector immune responses, thereby enabling tumor cells to evade immune-mediated destruction. Importantly, a higher baseline abundance of these immunosuppressive populations was predictive of poorer therapeutic outcomes, highlighting these cells as potential barriers to CAR T efficacy.

This study elucidates how the dynamic immune microenvironment within the central nervous system is a decisive factor shaping the success or failure of CAR T therapy in recurrent GBM. By capturing this immune modulation longitudinally through CSF sampling, the research offers a real-time window into the evolving battle between tumor and immune system—a feat rarely achievable in solid tumors due to the invasive nature of brain sampling.

Looking ahead, these insights pave the way for rational design of next-generation CAR T therapies optimized to overcome the suppressive tumor milieu. Strategies may include preconditioning regimens that selectively deplete Tregs or inhibitory myeloid cells before CAR T infusion, or genetically engineering CAR T cells “armed” with molecular tools to neutralize immunosuppressive signals locally within the brain. Such combinatorial approaches could potentiate better tumor control and durable remissions.

Furthermore, the deployment of CSF-based liquid biopsy techniques offers a transformative clinical tool for personalized monitoring. Tracking immune cell subsets and activation states could tailor therapeutic adjustments for individual patients, enabling precision immunotherapy guided by the tumor’s evolving immune landscape rather than static tissue biopsies.

Pending expanded evaluation in ongoing Phase I clinical trials (ClinicalTrials.gov identifiers: NCT07209241 and NCT05168423), this dual-target CAR T cell platform heralds a promising frontier in tackling GBM. It exemplifies how integrating advanced cellular therapies with in-depth immune profiling can elucidate resistance mechanisms and unlock pathways for clinical improvement in cancers once deemed intractable.

In sum, this research not only advances scientific understanding of CAR T mechanisms in solid malignancies but also offers hope for enhanced therapeutic strategies against one of the deadliest brain cancers. Elevating the endogenous immune compartment, particularly innate effectors like NK cells, represents a pivotal axis for augmenting CAR T cell efficacy and ultimately improving survival for patients battling recurrent glioblastoma.

Subject of Research: People

Article Title: The critical role of endogenous immune compartment after CAR T cell therapy in recurrent GBM

News Publication Date: Not specified

Web References:

• https://www.pennmedicine.org/news/dual-target-car-t-cell-therapy-slows-growth-of-aggressive-brain-cancer
• https://clinicalresearch.pennmedicine.org/us/en/listing/9046/upcc-10325-phase-ib-NCT07209241-696/
• https://clinicalresearch.pennmedicine.org/us/en/listing/7338/upcc-16321-phase-1-NCT05168423-696/

References: Published in Cell

Keywords: CAR T cell therapy, glioblastoma, recurrent GBM, cerebrospinal fluid, intracerebroventricular infusion, immune microenvironment, natural killer cells, regulatory T cells, immunosuppression, single-cell RNA sequencing, immunotherapy, personalized medicine

At the core of this study is the revelation that microglia, traditionally appreciated as passive immune responders, exhibit highly dynamic and context-specific behaviors that critically influence glioblastoma progression. These resident immune cells constantly patrol the brain’s parenchyma, scanning for abnormalities and potential threats. However, in the tumor context, microglia are far from mere bystanders; they actively engage with glioblastoma cells in a complex crosstalk that either restrains or facilitates tumor invasion, depending on the microenvironmental conditions. This discovery shatters longstanding assumptions about microglial roles in tumor biology and introduces new paradigms for therapeutic interventions.

The investigative team leveraged the cutting-edge technology of three-photon microscopy, which employs infrared light to penetrate deep into brain tissue with minimal phototoxicity. This technique allowed real-time, high-resolution visualization of cellular interactions several millimeters away from the dense tumor core, specifically focusing on the elusive far infiltration zone where individual tumor cells invade otherwise healthy tissue. This methodological advancement marks a significant departure from previous imaging techniques that were largely limited to superficial or excised tissue samples, providing an unprecedented window into glioblastoma’s invasive strategies within the living brain.

Intriguingly, the study documents a biphasic pattern of microglial behavior correlating with tumor progression stages. Initially, when only sparse glioblastoma cells have disseminated into the brain parenchyma, microglia become hyperactive, demonstrating increased motility and surveillance activity. This heightened state likely reflects an innate attempt by the brain’s immune defense system to contain the emerging threat. However, this vigilant immune response diminishes markedly as tumor infiltration intensifies, suggesting that glioblastoma cells may employ mechanisms to evade or suppress microglial vigilance, thereby facilitating unchecked invasion and growth.

An essential facet of the study involved dissecting the role of specific microglial receptors responsible for environmental sensing. By inactivating these receptors, researchers observed significant alterations in microglial behavior and, consequently, impacts on tumor cell invasion patterns. Complementing these experiments, pharmacological depletion strategies were applied to drastically reduce microglial populations within the tissue. These manipulations provided compelling evidence that modulating microglial function directly influences the ability of glioblastoma cells to invade distant brain regions, underscoring microglia as potential therapeutic targets.

The promising implications of these findings extend into the therapeutic sphere, where targeting microglial pathways pharmacologically could transform current treatment approaches. Dr. Felix Nebeling, lead author of the study, emphasizes the prospect that drugs modulating microglia behavior may constrain tumor spread, potentially improving patient outcomes in a disease where prognosis historically remains dismal. Importantly, this strategy deviates from conventional tumor-centric therapies by incorporating the brain’s immune microenvironment as a pivotal factor in disease modulation.

Beyond therapy development, this research enhances our fundamental understanding of glioblastoma biology. The notion that tumor-microglia crosstalk can either hinder or boost tumor dissemination indicates a highly plastic and context-dependent tumor microenvironment. This paradigm invites further exploration into molecular mediators governing this bidirectional communication, including chemokines, cytokines, and receptor-ligand interactions that shape microglial phenotypes and functions in tumor niches.

The far infiltration zone, once an elusive region due to technical imaging limitations and tissue accessibility, emerges from this study as a critical battlefield in glioblastoma invasion. By scrutinizing these peripheral zones, the researchers illuminate early invasive processes and microglial responses that may serve as biomarkers for intervention efficacy or tumor aggressiveness. Such regional specificity reinforces the need for localized therapeutic delivery techniques and precision medicine in combating brain tumors.

A broader implication of this study rests on the methodological innovation of three-photon microscopy itself. Its ability to interrogate intact brain tissue in vivo at remarkable depth and resolution heralds new avenues for neuroscience research beyond oncology. This approach allows for real-time mapping of cellular networks and interactions in complex brain environments, providing insights into neurodegenerative diseases, trauma responses, and neural circuit dynamics.

Moreover, the interinstitutional collaboration among DZNE, University Hospital Bonn, and ImmunoSensation reflects a multidisciplinary synergy critical to tackling complex neurological diseases. By integrating expertise in neurodegeneration, clinical oncology, and immunobiology, the team achieved a comprehensive investigation spanning molecular, cellular, and systems-level analyses. Such collaborative models are essential to drive the translational breakthroughs needed for devastating diseases like glioblastoma.

In conclusion, the presented study represents a paradigm shift in understanding glioblastoma invasion within the living brain. It highlights the critical and nuanced role of microglia in modulating tumor spread, moving beyond traditional views that regard these immune cells as passive. As investigations continue into the molecular underpinnings of tumor-immune interactions, this research paves the way toward innovative therapies that harness the brain’s own immune machinery to fight one of the most lethal cancers.

Subject of Research: Animals
Article Title: Microglia-glioblastoma crosstalk mediates glioblastoma invasion at the far infiltration zone
News Publication Date: 14-Apr-2026
Web References: https://www.dzne.de/en/, https://www.ukbonn.de/patient_innen/international/english/, https://www.immunosensation.de/publications/microglia-glioblastoma-crosstalk-mediates-glioblastoma-invasion-at-the-far-infiltration-zone, https://www.cell.com/immunity/home, http://dx.doi.org/10.1016/j.immuni.2026.03.010
Keywords: Brain cancer, Microglia, Optical microscopy, Cancer cells, Glioblastoma cells, Glioblastomas, Neurological disorders

Glioblastoma presents an exceptionally heterogeneous landscape, confounding effective treatment strategies. Traditional methods often overlook the tumor’s spatial and cellular diversity, limiting our understanding of how malignant cells and their microenvironment orchestrate aggressive behavior. By integrating 121 spatial transcriptomic datasets with detailed single-cell profiles, the study captures an unprecedented resolution of the tumor’s cellular architecture. This multi-modal approach enables the mapping of distinct malignant communities and their microenvironmental niches, which sustain and accelerate tumor growth.

Central to the study’s findings is the identification of four malignant cellular communities consistently observed across patients. These communities form spatially coherent clusters characterized by unique gene expression signatures and cellular behaviors. This discovery shifts the paradigm from viewing GBM as a monolithic mass to understanding it as a complex ecosystem, where cellular communities function dynamically in concert, shaping the tumor’s clinical characteristics.

Among these cellular communities, two distinct subpopulations of mesenchymal-like (MES-like) tumor cells stand out, highlighting the profound heterogeneity even within defined cell lineages. The first subpopulation, termed MES-Hyp, thrives in hypoxic niches and is anatomically interwoven with monocyte-derived brain macrophages. This spatial association hints at a collaborative interplay where immune cells may influence hypoxia-induced tumor evolution and resistance.

The second MES-like subpopulation, termed MES-Ast, exhibits a unique association with vascular elements such as endothelial cells, pericytes, and vascular smooth muscle cells. This cellular neighborhood suggests a role for MES-Ast cells in modulating the tumor vasculature, potentially facilitating nutrient supply and invasive growth. The dichotomy between MES-Hyp and MES-Ast not only underscores the complexity of mesenchymal tumor states but also their functional specialization within the tumor microenvironment.

Beyond the identification of these malignant communities, the study pioneers predictive and experimental validation of cell-type-specific ligand-receptor interactions. These intercellular communications represent molecular conversations that underlie tumor maintenance, immune evasion, and therapeutic resistance. By decoding these signaling networks within each community, the research uncovers previously unrecognized pathways that could be exploited for targeted disruption.

One of the study’s most striking revelations comes from patch sequencing, a technique that combines electrophysiology with single-cell profiling, applied here to tumors in situ. This enabled the discovery that synaptic-like connections between glioma cells and neurons predominantly involve oligodendrocyte-progenitor-like tumor cells (OPC-like). This novel insight suggests that glioma cells not only coexist but intimately interact with neuronal networks, potentially hijacking neural circuitry to support tumor growth and dissemination.

These synaptic interactions open a new frontier in understanding glioma biology, proposing that neural activity and tumor progression are tightly linked—a concept that may revolutionize treatment paradigms by targeting tumor-neuron communication. This insight dovetails with emerging evidence on the role of the nervous system in cancer, moving glioma research into an exciting new neuro-oncology era.

Together, the integrated multi-omic approach delineates a spatial and functional blueprint of the GBM microenvironment, revealing complex cellular ecosystems and dynamic intercellular crosstalk. This spatially resolved molecular atlas provides an invaluable resource for the academic and clinical community, offering maps of cellular states and interactions that drive malignancy and therapeutic resistance.

In clinical terms, these discoveries imply that targeting a single cellular population or signaling pathway might be insufficient, given the tumor’s community-based resilience. Instead, innovative combination therapies disrupting multiple malignant communities and their interactions with the microenvironment might be mandatory to achieve durable responses.

The study also highlights the critical role of tumor-associated macrophages in shaping the hypoxic niche and influencing mesenchymal tumor states, suggesting that modulating immune cell infiltration or function might impair tumor adaptation to harsh microenvironmental conditions and drug resistance.

Vascular-associated MES-Ast cells’ interactions with blood vessel components imply that disrupting tumor-perivascular niches could starve tumors of vital resources and block invasive fronts—potentially enhancing standard chemoradiotherapy efficacy.

Moreover, the identification of ligand-receptor pairs and intercellular communication pathways offers a treasure trove of novel molecular targets. Therapeutic interventions designed to block these molecular dialogs could dismantle the malignant communities’ cooperative networks, rendering the tumor more vulnerable.

This study represents a significant leap forward for personalized neuro-oncology, as the elucidated tumor microenvironmental landscapes differ between patients but maintain overarching cellular community themes. Such knowledge enables stratification of patients based on their tumor’s community composition, enabling precision medicine strategies tailored to disrupt specific pathological interactions.

Technological synergy among spatial transcriptomics, single-cell ATAC-seq to profile chromatin accessibility, and integrative multi-omics bioinformatics set a new standard for tumor microenvironment studies. This multifaceted approach facilitates the construction of a holistic tumor tissue atlas—spatially and functionally annotated at single-cell resolution.

The profound insights into glioblastoma’s cellular ecology gained from this study are expected to galvanize the development of next-generation therapeutic approaches that simultaneously combat tumor heterogeneity and the supportive microenvironment. As the fight against GBM continues, such spatially resolved single-cell analyses may unlock long-elusive vulnerabilities and engender strategies to outsmart this devastating disease.

Taken together, the methodological innovation and biological discoveries presented in this research represent a turning point in glioblastoma research. By unmasking the hidden world of malignant cellular communities and their intimate molecular dialogues, the study lays the groundwork for new therapeutic avenues that can reshape the landscape of brain cancer treatment.

Subject of Research: Glioblastoma tumor microenvironment, spatial transcriptomics, single-cell characterization, intercellular communication, tumor heterogeneity

Article Title: Spatial and single-cell characterization of human glioblastoma tumor microenvironment reveals malignant cellular communities.

Article References:
Lin, J., Chen, C., Li, S. et al. Spatial and single-cell characterization of human glioblastoma tumor microenvironment reveals malignant cellular communities. Nat Neurosci (2026). https://doi.org/10.1038/s41593-026-02265-5

DOI: https://doi.org/10.1038/s41593-026-02265-5

Glioblastoma multiforme (GBM) has long presented a grim prognosis, with less than 7% of patients surviving five years post-diagnosis, highlighting an urgent need for innovative therapeutic strategies. The resilience of GBM is partially attributed to its unique tumor microenvironment, where immune cells called microglia and infiltrating myeloid cells exert profound influences. These cells can create an immunosuppressive niche, enabling tumors to circumvent immune-mediated destruction despite conventional therapies. Until now, the molecular underpinnings orchestrating this immune evasion have been poorly understood.

The Northwestern team, led by assistant professor of neurological surgery Jason Miska, focused on the metabolic activity of microglia within glioblastoma. Unlike peripheral immune cells, microglia uniquely express GLUT5, a specialized transporter facilitating fructose uptake. This transporter’s expression suggested that fructose—a sugar commonly linked to inflammatory diseases outside the brain—may play a distinctive role in tumor-associated microglial function inside the brain milieu.

Employing sophisticated methodologies, including flow cytometry and single-cell genetic sequencing, the researchers meticulously analyzed cell populations harvested from mouse glioblastoma models. This systematic interrogation demonstrated that microglia, and microglia alone among immune cell types, possess the metabolic machinery to transport and metabolize fructose. This selectivity implicates fructose metabolism as a specific regulator of microglial behavior in the tumor environment.

To probe fructose metabolism’s role in glioblastoma progression, the investigators utilized genetically engineered mice deficient in the GLUT5 fructose transporter specifically in microglia. Remarkably, tumors in these transporter-deficient animals failed to grow, correlated with a marked enhancement in immune activity. Microglia became more inflammatory and produced cytokines that stimulate the proliferation and activation of CD8+ T cells — the immune system’s primary effectors against cancer. Such T-cell activation was closely tied to tumor rejection, underscoring the vital interplay between metabolic pathways and immune responses within the brain.

Leah Billingham, a postdoctoral fellow and co-first author, noted that this metabolic circuit not only modifies microglial function but orchestrates a broader immune network involving T and B lymphocytes. The synergy between these immune cells culminates in an environment hostile to tumor survival, revealing that metabolic inhibition of fructose uptake may reinvigorate anti-tumor immunity profoundly.

The discovery holds immense promise for overcoming the persistent challenge that glioblastoma poses to effective treatment. Despite medical advances, the standard-of-care therapies for GBM—including surgery, radiation, and chemotherapy—have remained essentially unchanged for two decades, with dismal improvements in survival. Targeting microglial fructose metabolism represents a paradigm shift, potentially arming clinicians with new tools to sensitize tumors to immunotherapies and conventional regimens alike.

Intriguingly, this research also highlights how the brain’s unique metabolic landscape differs fundamentally from other organs where fructose consumption is often linked to heightened inflammation, including conditions like colon cancer or diabetic neuropathy. Within the central nervous system, fructose metabolism paradoxically supports an immunosuppressive state that favors tumor growth, signifying that metabolic pathways are exquisitely context-dependent.

Looking ahead, the research team aims to identify pharmacological agents capable of selectively inhibiting GLUT5-mediated fructose uptake in microglia. Preclinical testing will evaluate whether these agents can synergize with existing brain cancer treatments or checkpoint blockade immunotherapies to enhance anti-tumor responses. Such combinatorial strategies could potentially translate into improved survival outcomes for patients facing glioblastoma.

Beyond therapeutic implications, this study enriches our broader comprehension of the metabolic crosstalk within the brain’s immune microenvironment. By unveiling fructose metabolism as a linchpin in microglial-mediated immunosuppression, the findings underscore metabolism’s role as not merely a biochemical process but a critical determinant of immune function and cancer progression.

This pioneering work was supported by an array of prestigious funding sources, including various National Cancer Institute grants, the Cancer Research Institute, and the National Institute of Neurological Disorders and Stroke. The team’s multidisciplinary approach, combining neurological surgery, immunology, and molecular biology, exemplifies the collaborative effort needed to tackle the formidable challenges posed by glioblastoma.

In summary, the identification of microglial fructose metabolism as essential for glioblastoma growth constitutes a landmark advance in neuro-oncology. By elucidating a previously unrecognized metabolic mechanism of immune evasion, this research not only provides a promising new target for drug development but also offers hope for more effective interventions against one of the most aggressive brain tumors afflicting humanity. As subsequent studies translate these insights into clinical innovations, patients and clinicians alike may anticipate a new era in which the metabolic manipulation of immune cells revolutionizes brain cancer therapy.

Subject of Research: Microglial fructose metabolism and its role in glioblastoma tumor growth and immunosuppression

Article Title: Microglial fructose metabolism is essential for glioblastoma growth

News Publication Date: 17-Mar-2026

Web References:
https://www.pnas.org/doi/10.1073/pnas.2521256123

References:
Miska, J. et al. (2026). Microglial fructose metabolism is essential for glioblastoma growth. Proceedings of the National Academy of Sciences.

Image Credits: Northwestern University

Keywords: Brain cancer, Glioblastomas, Glioblastoma cells, Microglia, Fructose