The authors organise the resistance problem into four interlocking dimensions. The first is physical and cellular: the blood–brain barrier and the blood–brain tumour barrier restrict what enters the brain, while once inside, tumour cells deploy ATP-binding efflux pumps that expel chemotherapeutics, sequester drugs in subcellular compartments where they cannot act, and metabolically inactivate agents before they reach their targets. The net effect is that intracellular concentrations of effective drug fall below therapeutic thresholds even when patients tolerate full systemic doses. Temozolomide, the backbone of glioblastoma care, illustrates the point vividly: the DNA-repair enzyme MGMT can directly reverse the drug’s methylation damage, and many tumours either express MGMT abundantly or acquire that capacity under treatment pressure.

The second dimension is molecular escape. Tumour genomes are not static; they repair DNA damage, mutate drug targets, amplify oncogenic drivers on extrachromosomal DNA — circular fragments of genetic material that exist outside the chromosomes and can carry dozens of copies of resistance genes — and rewire RNA splicing to produce protein variants that no longer recognise the drug. Extrachromosomal DNA has attracted particular attention because it can rapidly change copy number as selective pressure shifts, allowing tumour cell populations to dial oncogene expression up or down within a few cell divisions. Aberrant splicing similarly generates isoforms of kinases and receptors that lack the binding domains targeted by small-molecule inhibitors, rendering otherwise potent drugs blind to their intended substrate.

Third, the review catalogues intrinsic cellular drivers of resistance: cancer stem cells that persist in a dormant, quiescent state impervious to agents that kill dividing cells; subtype switching, in which tumour populations shift their transcriptional identity toward a more aggressive or less drug-sensitive state; epigenetic remodelling that silences pro-apoptotic genes; metabolic reprogramming that reroutes biosynthetic and energy pathways; and a broad resistance to multiple modes of cell death, not merely apoptosis. A glioblastoma cell that has downregulated its apoptotic machinery will survive a therapy designed to trigger it, which is why the authors emphasise that future treatments must engage alternative death programmes such as ferroptosis — iron-dependent lipid peroxidation — and pyroptosis, an inflammatory form of regulated necrosis.

The fourth dimension is the tumour microenvironment and its neural connections. Hypoxic regions reduce the efficacy of radiotherapy and many drugs; immunosuppressive cell populations, including myeloid-derived suppressor cells and polarised tumour-associated macrophages, blunt immune-based approaches; and exosomes shuttle resistance-conferring proteins and nucleic acids between cells. Perhaps most strikingly, the review highlights intertumoural neural-like physical networks — tumour cells connected by membrane tubes that share cytoplasmic content — and functional connections with host neurons, which facilitate both the spread of toxic signals and malignant regeneration after treatment. Brain tumours, in this view, are not merely collections of resistant cells but integrated tissues wired into the nervous system itself.

Against this formidable backdrop, the authors argue that nanomedicines offer a uniquely multidimensional counter-strategy. Nanoparticles can be engineered to cross the blood–brain barrier through receptor-mediated transcytosis, using ligands such as apolipoprotein E, transferrin or cyclic RGD peptides that hijack natural transport routes. Once across, they can be decorated with targeting moieties that promote uptake by tumour cells while bypassing efflux pumps, since particles are internalised intact rather than recognised as soluble substrates. Co-delivery is another central advantage: a single carrier can ferry a small-molecule inhibitor together with nucleic acid drugs — small interfering RNAs, microRNAs or even CRISPR components — to silence resistance pathways such as MGMT, PI3K signalling or Bcl2L12 at their genetic source, achieving combinations that would be pharmacologically difficult with free drugs.

The review then dissects five categories of nanosystems. Lipid-based carriers, including liposomes, solid lipid nanoparticles and nanostructured lipid carriers, are the most clinically mature; nanoliposomal irinotecan has already reached patients with glioma, and rhenium-186 nanoliposomes have been explored for brachytherapy-like localised irradiation. Polymeric nanoparticles built from PLGA, polycaprolactone or polyethyleneimine offer controlled release and robust nucleic acid loading. Inorganic platforms — mesoporous silica, gold nanostructures, carbon dots and magnetic iron oxide nanoparticles — enable physicochemical interventions such as photothermal therapy and photodynamic therapy, which use near-infrared light to generate lethal heat or reactive oxygen species and can inactivate thermotolerant, drug-resistant proteins that ordinary chemotherapy cannot touch. Hybrid lipid–polymer nanoparticles combine the stability of polymer cores with the biocompatibility of lipid shells, while bioderived and biomimetic systems — extracellular vesicles, cell-membrane-coated particles and bacterial outer membrane vesicles — exploit natural stealth properties to evade immune clearance and home to tumour tissue.

The authors are careful to temper enthusiasm with a candid accounting of defects. Carrier toxicity remains a concern, particularly for cationic materials such as polyethyleneimine; in vivo stability is undermined by protein corona formation and clearance by the reticuloendothelial system; scale-up from laboratory synthesis to Current Good Manufacturing Practice production is non-trivial for complex, multi-component particles; and clinical translation has been slowed by inconsistent targeting efficiency in human tumours, heterogeneity of the blood–brain tumour barrier across patients, and the difficulty of demonstrating intratumoural drug delivery non-invasively. Strategies for improvement discussed in the review include biomimetic camouflage, stimuli-responsive release triggered by tumour acidity or glutathione levels, microenvironment remodelling to normalise vasculature and relieve hypoxia, and switching cell death modality from apoptosis toward ferroptosis and pyroptosis to defeat apoptosis-resistant clones. Convection-enhanced delivery, which infuses therapeutic agents directly into brain tissue under pressure gradients, is presented as a complementary route that sidesteps the barrier entirely.

Ultimately, the review positions nanomedicine not as a single magic bullet but as a platform for rational, multi-pronged assault on resistance — breaching barriers, evading pumps, silencing escape pathways, applying physical energy, remodelling the microenvironment and reprogramming how tumour cells die. The authors frame their synthesis as a reference for both basic researchers designing the next generation of carriers and clinicians weighing which nanotherapeutic strategies are closest to meaningful clinical impact. For patients with resistant CNS tumours, whose options remain tragically narrow, the message is cautiously hopeful: the tools to systematically reverse drug resistance are being assembled, and the decisive question now is whether the field can carry them across the final, most difficult barrier of all — the distance from the laboratory bench to the clinic.

Subject of Research: Nanomaterial-based strategies to overcome therapeutic resistance in central nervous system tumours

Article Title: Nanomedicines for resistant tumours in the central nervous system: novel materials and mechanisms of action

Article References: Li, G., Chan, Y.-T., Xiong, F., Xin, Y., Hong, R., Xie, Z., Zhou, W., Zhang, C., Zhang, R., Wang, N., & Huang, Q. (2026). Nanomedicines for resistant tumours in the central nervous system: novel materials and mechanisms of action. Molecular Cancer. https://doi.org/10.1186/s12943-026-02783-7

Image Credits: AI Generated

DOI: 10.1186/s12943-026-02783-7

Keywords: nanomedicine, CNS tumours, blood-brain barrier, drug resistance, glioblastoma, ferroptosis, pyroptosis, lipid nanoparticles, biomimetic nanosystems, tumour microenvironment, clinical translation, chemoradiotherapy resistance

Gliomas, notorious for their resistance to conventional treatments such as chemotherapy and radiation, have posed significant challenges due to their complex biology and the sanctuary-like environment of the brain. The study delves deep into the molecular intricacies of regulated cell death—processes like apoptosis, necroptosis, and ferroptosis—that govern cellular fate within glioma tissues. By understanding how these pathways operate and are dysregulated in glioma cells, scientists can now strategically tip the balance towards cell death, effectively debilitating the tumor.

Central to this research is the concept that glioma cells, despite their resilience, rely heavily on evading regulated cell death to sustain uncontrolled proliferation. The authors meticulously dissected key signaling cascades that glioma cells hijack to suppress apoptosis and escape elimination. They discovered that reactivating these dormant death pathways through targeted molecules leads to selective tumor cell eradication, while sparing healthy brain tissue. This selective approach marks a significant departure from the often indiscriminate damage associated with current therapies.

The investigation further highlights the nuanced role of necroptosis, a form of programmed necrosis, in glioma cell dynamics. Unlike apoptosis, necroptosis triggers inflammatory responses, which the study suggests could be harnessed to stimulate immune-mediated tumor clearance. By employing experimental models, researchers demonstrated that inducing necroptosis within glioma microenvironments recruits immune cells, potentially converting immune evasion into an orchestrated attack against the tumor. This dual mechanism of direct cell death and immunomodulation could revolutionize glioma treatment paradigms.

Another facet of this comprehensive study focuses on ferroptosis—an iron-dependent form of regulated cell death characterized by lipid peroxidation. Gliomas exhibit heightened sensitivity to ferroptosis-inducing agents, providing a therapeutic window for intervention. The authors describe how manipulating iron metabolism and redox balance within glioma cells initiates ferroptotic cascades, culminating in cell membrane disruption and tumor demise. This discovery opens an exciting therapeutic avenue that harnesses metabolic vulnerabilities unique to gliomas.

The research paper does not shy away from the complexities posed by the blood-brain barrier (BBB), a formidable obstacle for drug delivery in brain cancer. Innovative strategies discussed include designing nanoparticles and molecular carriers capable of crossing the BBB to deliver cell death-inducing compounds directly to the tumor site. This targeted delivery system enhances the efficacy and reduces systemic toxicity, addressing a critical limitation in neuro-oncology therapeutics.

Furthermore, the study explores combinatorial approaches by integrating regulated cell death inducers with immune checkpoint inhibitors, capitalizing on the synergistic potential between direct glioma cell killing and immune activation. Such multi-pronged tactics could surmount the immunosuppressive microenvironment typical of gliomas, rendering them more susceptible to eradication. The synergy between these modalities embodies a forward-thinking model for personalized and adaptive therapy regimens.

Clinical relevance is underscored by preliminary data from patient-derived glioma models, where therapeutic interventions targeting cell death pathways exhibit promising tumor regression and prolonged survival. These findings set the stage for forthcoming clinical trials, elevating the translational impact of the research from bench to bedside. The hope is that these novel therapies will soon transition into standard care protocols, significantly improving prognosis and quality of life for glioma patients.

The researchers also emphasize the importance of biomarker development to monitor treatment response and predict sensitivity to regulated cell death modulation. Identifying biomarkers linked to apoptosis, necroptosis, and ferroptosis could facilitate patient stratification, allowing clinicians to tailor therapies based on individual tumor biology. This precision medicine approach enhances treatment efficacy while minimizing unnecessary exposure to ineffective drugs.

Of particular note is the technological prowess employed in the study, including advanced single-cell sequencing and live-cell imaging techniques. These cutting-edge tools enabled the dissection of cell death pathways at unprecedented resolution, revealing heterogeneity within glioma populations and shedding light on resistance mechanisms. Such technologies continue to push the boundaries of cancer biology and therapeutic innovation.

The authors also contemplate potential challenges in clinical application, such as tumor heterogeneity, adaptive resistance, and potential adverse effects of inducing inflammatory forms of cell death. They stress the necessity of rigorous safety evaluations and controlled clinical testing to balance therapeutic benefits against risks. This cautious optimism embodies responsible scientific advancement.

The study’s findings have broader implications beyond gliomas, offering insights into the role of regulated cell death in other neuro-oncological disorders and malignancies. The mechanistic frameworks established here could inform strategies across a spectrum of cancers, highlighting the universal relevance of targeting cell death pathways to overcome tumor resilience.

Notably, this research ignites a paradigm shift, advocating for a move from traditional cytotoxic agents toward biologically sophisticated, mechanism-based therapies. By exploiting the vulnerabilities inherent in glioma’s survival strategies, scientists are crafting a new arsenal equipped to dismantle these tumors at their core.

In summary, this comprehensive exploration into glioma vulnerabilities via regulated cell death pathways marks a thrilling milestone in cancer research. The convergence of molecular biology, immunology, and innovative drug delivery systems heralds a new era of targeted, effective, and personalized glioma therapy. As these groundbreaking approaches progress through clinical validation, they hold the potential to rewrite the prognosis for countless individuals afflicted by this devastating disease.

Subject of Research:
Article Title:
Article References:
Guo, J., Zong, L., Huang, Y. et al. Unlocking glioma vulnerabilities: targeting regulated cell death pathways for innovative therapies. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-02949-8
Image Credits: AI Generated
DOI: https://doi.org/10.1038/s41420-026-02949-8
Keywords:

Gliomas, which are among the most prevalent forms of brain tumors, present significant challenges due to their aggressive nature and variable prognosis. The traditional methods for diagnosing and treating gliomas often rely on histological analysis, imaging studies, and clinical assessments, which can be both time-consuming and fraught with limitations. The integration of AI offers a promising avenue for addressing these challenges by employing advanced machine learning techniques and data-driven approaches to optimize both diagnosis and therapeutic strategies.

One of the breakthrough aspects of AI in glioma research is its ability to analyze vast datasets with unparalleled speed and accuracy. Algorithms can efficiently sift through complex medical imaging, such as MRI scans, to identify patterns and subtle distinctions that might elude even the most seasoned radiologist. The systematic review elucidates numerous studies demonstrating how AI models trained on expansive datasets can achieve comparable or even superior accuracy rates in tumor detection compared to human specialists.

Moreover, AI can assist in differentiating between various subtypes of gliomas, which is crucial for treatment planning. For instance, the genetic makeup and molecular subtype of a glioma can dictate its responsiveness to different therapies. AI algorithms can analyze genomic data alongside imaging results, creating a more comprehensive view of the tumor that allows for tailored approaches to treatment. This ability to personalize therapy represents a significant advancement toward precision medicine.

In addition to diagnostics and treatment personalization, the systematic review emphasizes the role of AI in predicting treatment responses. By leveraging historical patient data and outcomes, AI systems can forecast which patients are likely to respond favorably to specific therapeutic interventions. Such predictive capabilities enable oncologists to make more informed decisions and potentially avoid ineffective treatments, thus saving patients from unnecessary side effects and improving their quality of life.

Another critical area of focus in the review is the incorporation of AI in the field of radiotherapy. Radiotherapy remains a cornerstone in managing patients with gliomas, but planning treatment strategies can be intricate and labor-intensive. AI-driven tools allow for automated treatment planning, which enhances accuracy and can lead to more effective radiation delivery. These advancements not only maximize tumor targeting but also minimize damage to surrounding healthy tissues, a significant factor in preserving neurological function.

The review also underlines the collaborative potential of AI in fostering interdisciplinary research. By bridging the gaps between radiology, pathology, and neurology, AI paves the way for integrated approaches that can enhance our understanding of glioma biology and treatment responses. Collaborative efforts that incorporate AI technologies can lead to more comprehensive strategies for tackling gliomas, ultimately benefiting patient care.

However, the integration of AI in clinical settings is not without its challenges. Data quality, ethical considerations, and the need for regulatory standards are paramount concerns that must be addressed as AI becomes more prevalent in glioma research and treatment. Robust datasets are necessary for training AI algorithms effectively, and ensuring the authenticity and diversity of these datasets is critical for minimizing biases that could impact patient care.

Moreover, as AI systems become sophisticated tools in clinical decision-making, the implications for medical ethics come to the forefront. How much autonomy should physicians relinquish to AI systems? Ensuring that AI serves as a supportive tool rather than a replacement for human expertise is essential in maintaining the physician-patient relationship grounded in trust and empathy.

Despite these challenges, the potential benefits of AI in the realm of gliomas cannot be overstated. As our understanding of AI technology continues to evolve, we witness an exciting era where machine learning models can complement human decisions, resulting in more effective and timely interventions. The systematic review accentuates that ongoing research and trials will further elucidate the optimal ways to deploy these technologies, ensuring that glioma patients benefit from rapid advancements in artificial intelligence.

The systematic review by Karavolias and Mammis thus provides a comprehensive overview of a rapidly evolving field, charting the course for future research and potential clinical applications. This works encourages both researchers and clinicians to explore collaborations that leverage AI’s capabilities, and stresses the importance of adapting quickly to technological advancements to meet the needs of patients facing glioma diagnoses.

Drawing from this review, one can speculate on the future landscape of glioma treatment with AI at its helm. As we continue to harness the power of artificial intelligence, not only do we improve the diagnostic process, but we also open new avenues for innovative treatment modalities. In this light, the relentless pursuit of integrating AI into the medical field stands as a beacon of hope for countless patients battling gliomas and other malignancies.

The marriage of artificial intelligence and glioma research presents a narrative of optimism, resilience, and unwavering human effort. As the scientific community expands its horizons, embracing the advancements offered by AI and machine learning, we edge closer to a world where gliomas can be diagnosed earlier, treated more effectively, and managed with a patient-centric approach that prioritizes outcomes and quality of life.

Through systematic reviews like that of Karavolias and Mammis, it is clear that as we venture deeper into the realm of AI, the impact on glioma diagnosis and therapy will not only be profound but transformative for the recipients of such advancements.

Subject of Research: Emerging artificial intelligence research in glioma diagnosis and therapy.

Article Title: Systematic review of emerging artificial intelligence research in glioma diagnosis and therapy.

Article References:

Karavolias, I., Mammis, A. Systematic review of emerging artificial intelligence research in glioma diagnosis and therapy.
Discov Artif Intell (2026). https://doi.org/10.1007/s44163-025-00640-y

Image Credits: AI Generated

DOI: 10.1007/s44163-025-00640-y

Keywords: glioma, artificial intelligence, diagnosis, therapy, machine learning, personalized medicine, radiotherapy, predictive analytics.

Gliomas, as primary brain tumors notorious for their heterogeneity and therapeutic challenges, have long withheld a comprehensive understanding of exploitable molecular weaknesses. Among these, the loss of methylthioadenosine phosphorylase (MTAP) homozygous deletion emerges as a recurrent genomic alteration, intimately linked with tumor metabolism and proliferation. MTAP encodes an enzyme pivotal in the methionine salvage pathway, and its absence triggers a cascade of metabolic adaptations within tumor cells. The research team has adroitly leveraged this metabolic frailty by exploring enzymes functionally intertwined with MTAP’s biological role, specifically PRMT5 and MAT2A.

Protein arginine methyltransferase 5 (PRMT5) is a symmetric dimethylarginine methyltransferase that has garnered attention for its multifaceted roles in gene regulation, RNA splicing, and epigenetic modification, all of which converge on oncogenic processes. Meanwhile, methionine adenosyltransferase 2A (MAT2A) catalyzes the critical synthesis of S-adenosylmethionine (SAM), a universal methyl group donor indispensable for myriad methylation events, including those mediated by PRMT5. MTAP deficiency leads to accumulations of methylthioadenosine (MTA), a natural PRMT5 inhibitor, rendering MTAP-deficient cells exquisitely sensitive to alterations in methionine metabolism and methylation dynamics.

By employing a combination of biochemical assays, genetic knockdowns, and pharmacological inhibition in MTAP-negative glioma models, the researchers demonstrate a synergistic lethality that far exceeds the additive effects of targeting either PRMT5 or MAT2A individually. This synthetic lethality culminates in profound impairment of glioma cell viability, characterized by disruptions in RNA splicing fidelity, epigenetic reprogramming, and the global methylome. Such cellular derailments trigger apoptosis and halt tumor progression, underscoring the efficacy of dual enzymatic targeting.

Integral to this discovery is the elucidation of the mechanistic underpinnings driving this vulnerability. The study highlights that inhibiting MAT2A diminishes intracellular SAM levels, effectively throttling methylation reactions catalyzed by PRMT5. Concurrently, PRMT5 inhibition compounds methylation deficits and disrupts essential gene regulatory networks. In MTAP-null cells, where the endogenous MTA-mediated inhibition of PRMT5 has already compromised methylation capacity, the combined therapeutic assault triggers a metabolic and epigenetic catastrophe unattainable by single-agent interventions.

The implications of these findings extend beyond the molecular intricacies. Targeting metabolic and epigenetic dependencies paves the way for precision oncology strategies tailored to the genetic landscape of tumors. The research conspicuously positions PRMT5 and MAT2A as actionable drug targets, especially given the availability of small molecule inhibitors currently progressing through clinical pipelines. Thus, the translational potential of this combination therapy offers a beacon of hope for patients afflicted with MTAP-deficient gliomas, a cohort that historically faces limited therapeutic options and unfavorable prognoses.

Moreover, the investigation employed state-of-the-art glioma models that faithfully recapitulate the genomic and phenotypic nuances of MTAP deletion, ensuring that the therapeutic insights bear clinical relevance. Through rigorous in vitro and in vivo validations, the combined PRMT5 and MAT2A inhibition manifested in tumor growth retardation, reduced proliferative indices, and increased apoptotic markers. This robust experimental design fortifies the credibility of synthetic lethality as a viable intervention in this oncologic context.

Intriguingly, the study sheds light on the broader landscape of metabolic-epigenetic interplay in cancer. It underscores how tumor cells, bound by their metabolic adaptations, can be selectively targeted by exploiting bottlenecks in their methylation machinery. This paradigm transcends gliomas, suggesting the potential applicability of similar synthetic lethality frameworks in other MTAP-deficient malignancies, such as pancreatic and lung cancers, which frequently exhibit comparable genomic deletions.

Furthermore, the exploration of downstream effects revealed perturbations in critical cellular pathways integral to RNA processing and chromatin remodeling. Aberrant splicing induced by PRMT5 and MAT2A inhibition generates defective transcripts, which accumulate and trigger cellular stress responses. The epigenetic derangements also unleash transcriptional silencing and activation shifts in tumor suppressor genes and oncogenes, tipping the cellular milieu towards apoptosis. These multifactorial disruptions converge into a molecular milieu hostile to sustained tumor survival.

The research team’s methodological rigor is noteworthy, harnessing cutting-edge transcriptomic and proteomic assays to map the extensive downstream ramifications of enzyme inhibition. High-resolution mass spectrometry-based methylome analyses elucidated differential methylation landscapes, while RNA sequencing captured the spectrum of splicing anomalies. Collectively, these data illuminate the complexity of the cellular response and affirm that targeting metabolic hubs can reverberate through diverse oncogenic pathways.

An additional compelling facet of this study is the potential to circumvent the notorious blood-brain barrier (BBB) challenge endemic to glioma therapeutics. The investigators conducted preliminary pharmacokinetic evaluations of MAT2A and PRMT5 inhibitors demonstrating favorable brain penetration profiles, a critical prerequisite for therapeutic efficacy in central nervous system malignancies. Such findings propel this synthetic lethality approach closer to clinical feasibility, addressing one of the major hurdles in neuro-oncology drug development.

Notably, the research delineates a therapeutic window rooted in the genetic stratification of gliomas. By focusing on tumors harboring homozygous MTAP deletions—a discrete molecular subset—the treatment approach minimizes collateral toxicity on normal tissues, which maintain intact MTAP functionality and thus withstand enzyme inhibition. This precision targeting reduces the risk of adverse effects and enhances the prospect of combinatorial regimens with existing standard-of-care therapies such as temozolomide or radiotherapy.

In addition, the dynamic interplay between metabolic inhibition and immune modulation emerges as an intriguing avenue for future exploration. The methylation alterations induced by PRMT5 and MAT2A inhibition may reshape the tumor immune microenvironment, potentially enhancing immunogenicity or sensitizing gliomas to checkpoint blockade therapies. Although this dimension extends beyond the current work, it paves the way for integrative treatment modalities blending metabolic targeting with immunotherapy.

Beyond therapeutic considerations, this discovery enriches the fundamental cancer biology field by exemplifying the concept of synthetic lethality leveraged through metabolic vulnerabilities. It echoes the emerging trend of targeting epigenetic regulators in cancer, expanding the armamentarium of anti-cancer strategies beyond classical genotoxic agents. This research epitomizes how dissecting tumor metabolism unlocks new frontiers in combatting recalcitrant malignancies.

As the study circulates through scientific and clinical circles, anticipation builds for subsequent clinical trials aimed at validating safety, efficacy, and optimal dosing regimens for the dual inhibition approach. The development of robust biomarkers for patient selection and treatment monitoring also represents a pivotal forthcoming endeavor, essential for translating these laboratory insights into tangible patient benefits.

In conclusion, this landmark study spearheaded by Jiang, Li, Xiao, and colleagues presents compelling evidence that combinatorial targeting of PRMT5 and MAT2A exploits a unique synthetic lethality in MTAP homozygous-deficient gliomas, marking a significant stride in precision neuro-oncology. Through meticulous elucidation of metabolic and epigenetic interplay, the research charts a promising course toward novel, efficacious therapies against a formidable class of brain tumors, potentially reshaping clinical management and improving patient outcomes in the near future.

Subject of Research: Combined enzymatic inhibition of PRMT5 and MAT2A to induce synthetic lethality in MTAP homozygous-deficient glioma models.

Article Title: Combined inhibition by PRMT5 and MAT2A demonstrates a strong synthetic lethality in MTAP homozygous-deficient glioma models.

Article References:
Jiang, Z., Li, X., Xiao, Z. et al. Combined inhibition by PRMT5 and MAT2A demonstrates a strong synthetic lethality in MTAP homozygous-deficient glioma models. Cell Death Discov. 11, 261 (2025). https://doi.org/10.1038/s41420-025-02545-2

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-025-02545-2